New Autoimmune Diseases Cure

The Autoimmune Bible System

The Autoimmune Bible system was developed by Mark Steve, who was suffering from an autoimmune disease that is not treatable. He tried other medicine and did not work, but after turning to the Bible, he was able to get the best healing for the disease. The product discusses in detail the Bible recipes and also the ingredients which come with it, which can be used to fight the diseases. God has provided the people with healing through the readily available things which can be found in the grocery, and it only needs one to follow them strictly, and you will get healed. The Bible has specific herbs, which it has mentioned, which could be used to heal the various disease which we are suffering which include the autoimmune disease and diabetes which continue to be a problem to many. The program can be accessed through the e-book, and some bonuses come with the program and maximum benefits from the program. You don't need any technical skills or other intermediate skills to use the product since it entails using the Bible. Read more here...

The Autoimmune Bible System Summary


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All of the information that the author discovered has been compiled into a downloadable pdf so that purchasers of The Autoimmune Bible System can begin putting the methods it teaches to use as soon as possible.

As a whole, this e-book contains everything you need to know about this subject. I would recommend it as a guide for beginners as well as experts and everyone in between.

Altered Balance Between Natural Treg and Self Reactive T Cells as a Possible Cause of Autoimmune Disease

The above findings in rodents and humans indicate that, in general, any genetic abnormality or environmental insult can be a cause or a predisposing factor of autoimmune disease if it affects the development, maintenance, and As examples of such genetic causes, defects of the Foxp3, CTLA-4, CD40, IL-2, CD25, or CD122 genes elicit severe autoimmune diseases in rodents and humans presumably through impairing the generation or function of natural CD25+CD4+ Treg, as discussed above. This also suggests that the polymorphisms of these genes may contribute to determining the genetic susceptibility to autoimmune disease by affecting Treg development or function. For example, the polymorphism of the IL-2 and CTLA-4 genes, which are known to associate with genetic susceptibility to T1D in NOD mice and humans 44,45 , may affect natural Treg-mediated mechanism of self-tolerance, as neutralizing anti-IL-2 antibody or blocking anti-CTLA-4 antibody exacerbate T1D in NOD mice, in part, by affecting...

Hypothesis on the Cause and Mechanism of Autoimmune Disease

The findings discussed above lead to formulation of a possible mechanism of autoimmune disease. That is, the development of many, if not all, autoimmune diseases, especially organ-specific ones, may be determined by two elements one is the degree of deficiency or dysfunction of natural Treg, or the balance between natural Treg and self-reactive T cells, and the other the host genes, including MHC and non-MHC genes, which determine the phe-notype of the autoimmune disease including the specificity and intensity of the autoimmune responses triggered by abnormal Treg cell-mediated control. This possible pathogenetic mechanism of autoimmune disease has the following implications. First, unless the abnormality of Treg is present, host genes per se are unable to cause autoimmune disease for example, mothers of IPEX patients are completely healthy even if they share phenotype-determining genes with their affected children 41 . Second, the degree of the abnormality of Treg is able to...

Mechanisms of Thyroid Autoimmunity

The other known genetic loci associated with thyroid autoimmunity, namely HLA, CTLA-4 and PTPN22, are shared between these 2 thyroid conditions, as well as many other autoimmune diseases reviewed in 3 . Several environmental factors have been delineated but some of these remain controversial and of unknown action, such as smoking and stress 4, 5 . Evidence for the involvement of infections is lacking (thyroid autoimmunity rarely follows subacute thyroiditis, for instance), but there does appear to be an association between congenital rubella infection and subsequent thyroid autoimmunity 6 . Genetic and environmental factors predispose to autoimmune disease through their effects on immunological tolerance (table 1). It is well established that most autoreactive T cells are deleted in the thymus, and this involves the intrathymic expression of self-antigens during development. This process is most clearly demonstrated in autoimmune polyglandular syndrome type 1, in...

Lack of Autoimmunity After Innate Overactivation A Role for Interferons and the Nervous System

Taken together, innate immunity typically results in two rather opposing consequences mostly, adaptive immune responses are favored. However, in case of inappropriate innate overimmunity, immuno-suppression is induced, meaning that adaptive immune responses are greatly suppressed. This may partly explain why severe burn injuries or acute pancreatitis are not regularly followed by autoimmune disease, despite the potential systemic release of autoantigens by tissue destruction. Rather, vigorous innate immune activation during such states is linked to an immunosuppression with a great risk of superinfection, sepsis, and death.

Autoreactivity and Conversion to Autoimmune Disease

Once autoantigen becomes systemically released, innate immunity is induced and adaptive responses therefore primed, the described criteria of autoreactivity are fulfilled. Autoreactivity describes a state where adaptive autoimmune responses (T cells and or autoantibodies) are measurable however, overt disease is still absent. This state can be observed in patients where autoreactive T cells are detectable years before onset of disease. Also, detection of autoantibodies is often possible in healthy persons without any further signs of autoimmune disease. In general, this may reflect a quality or quantity of the autoimmune responses below a threshold required for initiation of disease 65 . Furthermore, the conversion of autoreactivity into overt autoimmune disease requires additional immunological and inflammatory processes. First, autoreactive T cells have to be recruited to the peripheral target organ. Here, expression and function of chemokines and their respective receptors play an...

Regulatory Mechanisms in Autoimmunity

Supposing that autoimmunity is not the root cause of a disease, does that end the matter Even when the production of autoantibodies or autoreactive T cells clearly depends on the continued presence of the infecting organism or its residual antigen, it would be rash to conclude that self-antigens play no part. Their involvement might be secondary resulting from any of several known mechanisms, including epitope spreading 37, 91 , polyclonal activation of T or B cells by parasite mitogen 23 , and loss of downregulation 84 . Earlier discussions of downregulation have been superseded by the discovery of the new mechanisms listed in Table 2, all of which play a role in TCR-transgenic models of autoimmunity as shown. In humans, inactivation of the Treg marker FoxP3 gene causes the IPEX (immune dysregulation, polyen-docrinopathy, enteropathy, X-linked syndrome) syndrome 6 . The role of the adaptor molecule Cbl-1 in modulating autoimmunity is particularly well mapped out. Additional but less...

Disturbed Homeostasis of Peripheral B Cells in Autoimmune Diseases

Immunophenotyping of circulating B cells in patients with systemic autoimmune diseases has identified a number of specific abnormalities and may provide novel approaches in diagnosis as well as analysis of the response to therapeutic interventions (Odendahl et al. 2000a, b 2003 Hansen et al. 2002b Jacobi et al. 2003 Anolik et al. 2004 Looney et al. 2004a, b Cappione et al. 2002 Potter et al. 2002 Bohnhorst et al. 2001, 2002). Since B cells at many stages of development circulate in the blood and the stages of B cell development can be assessed using a number of phenotypic markers (Fig. 1), analysis of the expression profile of circulating B cells permits the detection of B cell differentiation status in health and disease. In the peripheral blood of healthy controls, approximately 60 -65 of B cells have the phenotype of CD27-na ve cells, and 30 -40 have that of memory B cells (CD27+). Typically, in such healthy donors, less than 2 of the peripheral B cells are plasma cells (CD19dim,...

AID in Aging and in Autoimmune Disease

A surprising finding in recent years was the discovery that even moderate changes in AID levels, either through alleles carrying function-altering mutations in heterozygotes or through changes in its regulation, have a significant impact in class switch recombination and somatic hypermutation. In this chapter, we examine the impact of the alteration of AID levels in two aspects of human health in aging and its potential association to age-related immunodeficiency, and in autoimmune disease. In the first section, evidence is discussed that strongly implicates decreased AID levels as a contributing factor for the suboptimal humoral responses in aged individuals. The second part of this chapter discusses the impact of altering AID levels in autoimmunity. Interestingly, any alteration in the levels of this protein in humans, in either direction, appears to be associated with a higher incidence of autoimmunity. This is not the case in mice, where lower levels of AID are associated with a...

Cellular Signal Transduction Pathways and Their Implications for Autoimmunity

The immune system is maintained by a fine balance between activation and inhibition (Fig. 2). On the one hand, it must possess adequate reactivity to generate an effective class="intexttaglink" data-tid="5690" href="/immune-response.html">immune response to target non-self molecules, while avoiding the emergence of autoimmunity on the other hand. Essential to this process is the ability to control the timing and site of B cell activation and to limit the extent of activation precisely. All of this is sufficiently regulated by a number of extrinsic and intrinsic mechanisms in a normal immune system to avoid pathogenic autoimmunity. It is currently believed that failure to maintain this balance of activating and inhibiting factors, receptors and pathways could result in either immunodeficiency or autoimmunity. marrow and in the peripheral lymphoid tissues, such as the spleen and lymph nodes. These checkpoints are necessary to produce a diverse population of B cells capable of generating high-affinity effector antibodies in the absence of pathologic...

AID deficiency and autoimmunity in humans

Unlike its mouse counterpart, AID deficiency in humans is associated with an increase in the incidence of certain autoimmune disorders, particularly the immune cytopenias, such as autoimmune hemolytic anemia, autoimmune thrombocytopenia or autoimmune neutropenia (Quartier et al., 2004). Interestingly, these autoimmunities are also associated with other primary immunodeficiencies such as common variable immune deficiency, and rarely, severe combined immunodeficiency (Arkwright et al., 2002). The common denominator appears to be the inability of the immunodeficient individual to clear persisting pathogens (Arkwright et al., 2002). It is possible that in those individuals with a residual lymphocyte population, there is compensation by relaxing tolerance checkpoints in order to deal with the pressure from persisting infection, allowing expansion and activation of autoreactive lymphocytes that would otherwise be prevented from participating in the immune response. It was also suggested...

Self Tolerance Maintained by Thymus Produced Natural Treg Induction of Autoimmune Disease by Their Manipulation at the

As evidence for the crucial role of natural Treg in the maintenance of natural self-tolerance, autoimmune diseases immunopathologically resembling their human counterparts can be produced in normal rodents by removing natural Treg from the periphery, abrogating their thymic production, or altering their survival or function at the molecular level. Induction of Autoimmune Disease in Normal Rodents by Depleting Treg from the Periphery Several lines of investigations suggested that T cells capable of preventing the development of autoimmune disease are present in normal animals 7 . For example, autoimmune disease spontaneously develops in mice that have received thymectomy in a critical neonatal period (day 2-4 after birth, see below) or in rats that are subjected to thymectomy in adults and several subsequent doses of X-irradiation the development of autoimmune disease in these animals can be prevented by inoculation of T cells, especially CD4+ T cells from histocompatible normal mice...

Therapies Targeting Autoimmunity

Traditional therapies for autoimmune neuropathies have proven beneficial for certain types of diabetic neuropathy (94). Plasmaphoresis and steroidal anti-inflammatories should be considered if the diagnosis is proximal diabetic neuropathy (diabetic amyo-trophy) or demyelinating neuropathy. Failure of these treatments or evidence of autoimmunity in typical diabetic polyneuropathy might warrant anti-immune approaches. Immune intervention with human intravenous immunoglobulin (IVIg) has become appropriate in some patients with forms of peripheral diabetic neuropathy that are associated with signs of antineuronal autoimmunity (94,95). Chronic inflammatory demyelinating polyneuropathy associated with diabetes is particularly responsive to IVIg infusion. Treatment with immunoglobulin is well tolerated and is considered safe, especially with respect to viral transmission (96). The major toxicity of IVIg has been an anaphylactic reaction, but the frequency of these reactions is now low and...

The Role of Host Genes in Determining the Phenotype of Autoimmune Disease

Determine which organs or tissues are targeted by the responses 52, 53 . The genetic class="intexttaglink" data-tid="15506" href="/makeup.html">makeup of the host mainly determines the phenotype of the autoimmunity triggered by altered T cell regulation. For example, NTx predominantly produces autoimmune oophoritis in the A strain, autoimmune gastritis in the BALB c but not DBA 2 strain (which shares the H-2d MHC haplotype), and no apparent organ-specific autoimmunity in the C57BL 6 strain 53 . Administration of neutralizing anti-IL-2 mAb produced gastritis in BALB c mice, exacerbated T1D in NOD mice 25 , and produced de novo autoimmune peripheral neuritis in NOD mice 25 . ATx and subsequent fractionated X irradiations predominantly induces thyroiditis in PVG c rats with the RT1c MHC haplotype, and T1D in MHC congenic PVG-RT1u rats 54 . Thus, MHC and non-MHC genes contribute to determining the phenotype of autoimmune disease triggered upon reduction or dysfunction of natural Treg. Polymorphisms of these genes may affect the formation of a...

Fear of Autoimmunity Can Hold Up Vaccine Development

On a more negative note, a mistaken belief in autoimmunity can hold up vaccine development, as Kierszenbaum cogently argues for Chagas' disease 63 . This is a disease where a vaccine is much needed high disease prevalence in particular areas, lack of effective symptomatic treatment and lack of effective anti-parasite measures. Meningococcus B is another instance. Conjugate vaccine against Meningococcus C composed of capsular polysaccharide conjugated to a protein carrier is effective and now widely used. A similar vaccine against Men B has not been developed because of the danger presented by expression of a cross-reactive polysaccharide in neural tissue (Table 5). Instead, several serogroup B vaccines based on outer membrane vesicles have been shown to be immunogenic and reasonably effective in adults and older children, but the protection offered by them is chiefly strain-specific. Table 5 Where threat of autoimmunity impedes vaccine development Table 5 Where threat of autoimmunity...

Inhibitory Receptor Pathways and Autoimmunity

Inhibitory receptors control the activation threshold of many immune cells, including B cells. There are many similarities in the signalling pathways of these inhibitory receptors. Inhibitory receptors also have specific effects, as they bind different ligands, and signal through different phosphatases. Consistent with a role of defects in inhibitory receptor function in autoimmunity is the finding that B cells from inhibitory receptor-deficient mice have similarities in phenotype and lowered thresholds for activation to those reported for B cells from SLE patients. Consistent with its role in mediating inhibitory receptor function, SHP-1 deficiency results in the development of spontaneous autoimmune disease. SHP-1 also associates with BCR, Fc, growth factor, complement and cytokine receptors (Shultz et al. 1984). SHP-1 knockout mice have a phenotype consistent with a prominent role of this tyrosine phosphatase in inhibitory receptor pathways (Sidman et al. 1986 Yu et al. 1996)....

The Thyroid and Autoimmunity in Children and Adolescents

Thyroid autoimmunity is the commonest disease process to affect thyroid function. The prevalence of thyroid autoimmunity increases throughout life, with a possible decline in frequency in the very old as a 'healthy survivor' effect. The mere presence of thyroid autoimmunity, as demonstrated by the presence of thyroid autoantibodies or focal thyroiditis, for example, does not equal thyroid disease, since the majority of people with focal thyroiditis do not become hypothyroid 1 . On the other hand, as far as we know the formation of thyroid-stimulating antibodies (TSAb) leads to Graves' disease in the great majority of subjects, even if in rare cases their levels may oscillate and be associated with a fluctuating clinical course. After a brief review of the basic immunological mechanisms which underlie autoimmune thyroid diseases, this chapter will focus on the comparatively few studies which have looked specifically at the pathogenic mechanisms in these disorders in children and...

Myasthenia Gravis

For myasthenia gravis, there are not so much diagnostic criteria as a set of diagnostic tests with varying sensitivity and specificity. These tests include characteristic clinical course, response to In the diagnostic criteria for neuropsychiatry systemic lupus erythematosus (one of many disorders associated with myasthenia gravis), there are diagnostic criteria for myasthenia gravis, but the extent to which the wider medical community or specialists in neuromuscular diseases adhere to this case definition is unclear.

Future Perspectives

Some of the initial studies on molecular mimicry and virus-induced autoimmunity indicated that viruses share common sequences with host components. It has been demonstrated that some viruses have acquired host genes and modified these to subvert the immune system. Herpesviruses encode MHC-like molecules, Fc receptors, IL-10-like factor and complement regulatory proteins, and poxviruses have incorporated into their genome, IL-1 receptor, tumor necrosis factor (TNF) receptor, IFN-y receptors and complement control proteins. In addition, viral proteins need to perform specific functions in the cell to replicate its genome and assemble new virions. These functions use the existing cellular machinery and therefore mimic many of the host cells, which also perform similar tasks. The key question is still how are these infections which are associated with autoimmune disease able to initiate the pathway leading to self-reactive immune responses

Negative and Positive Selection and Ignorance of the Developing Immature B Cell Repertoires

Genetic deficiencies in complement components such as CIq, C4, serum amyloid protein, and complement receptor 2 (CR2), as well as secreted natural serum IgM (Boes et al. 1998,2000 Chan et al. 1999), lead to systemic autoimmune disease (systemic lupus erythematosus, SLE) with a preponderance of autoantibodies against single- and double-stranded DNA and a variety of other nuclear antigens. Such high avidity autoantibodies are not found in normal, nondiseased individuals.

Fetal Thyroid Development and Function

Fertility is impaired in hypothyroid women with autoimmune thyroid disease and if such patients do achieve pregnancy the hypothyroid state is associated with a higher incidence of miscarriage early in pregnancy reviewed in 14 . Thyroid autoimmunity, as evidenced by the presence of anti-thyroid antibodies, present during early pregnancy even in the euthyroid situation, is associated with an increased risk of subsequent miscarriage 25 . Thyroid autoantibody positive women miscarry at a rate of between 13 and 22 compared to 3.3-8.4 in control euthyroid antibody negative women 14 . While the association between thyroid antibodies and miscarriage is strong that between these antibodies and recurrent abortion is less so. In the euthyroid woman with thyroid antibodies no specific treatment can be offered to reduce the antibody titres one uncontrolled study in euthyroid thyroid antibody positive women with recurrent abortion reported a significant success rate with thyroxine administration 26...

Autoreaction Rescued by Ignorance

How frequently are double producers selected into the BI or the conventional B cell compartments Do double producers also emerge from VH to DHJH rearrangements and are they positively selectable by mixtures of ignorant and autoreactive VH domains It also remains to be seen whether such double BcR-producers constitute a potential danger for autoimmune reactions and autoimmune diseases.

Cavernous sinus and orbital processes

An autoimmune disorder in which the extraocular muscles are enlarged and infiltrated with inflammatory elements, eventually leading to a restrictive oculomyopathy and motility disorder. The onset of the ensuing painful exophthalmos and chemosis, diplopia and lid retraction is rapid. The clinical picture needs to be differentiated in adults the condition results from idiopathic orbital inflammation, and in children it is caused by rhabdomyosarcoma or orbital cellulitis Myasthenia gravis

Conclusion and Perspective

There is now substantial evidence in animals and humans that naturally arising Treg play crucial roles in the maintenance of immunologic self-tolerance and their abnormality can be a cause of autoimmune disease. Further study of Treg, especially the molecular basis of their generation, activation, and function, will contribute to our understanding of the cause and mechanism of autoimmune disease. Furthermore, in addition to the present method of treating autoimmune disease by physically destroying autoimmune effector T cells as much and as specifically as possible, use of Treg may be a future strategy for the treatment and prevention of autoimmune disease through reestablishing dominant self-tolerance.

Gender Ethnicracial And Life Span Considerations

Cushing's syndrome in infants usually results from adrenal carcinoma. Primary disease is often linked to a familial autoimmune disorder and is seen in children and young adults of both genders. Secondary disease is more common than primary disease in children older than 6 or 7 and, as in adults, is usually the result of overproduction of ACTH. In adults, secondary Cushing's syndrome that results from pituitary disease is most common in females aged 30 to 50 years. Secondary Cushing's syndrome that results from increased ACTH secretion is more common in males, possibly because of the higher incidence of bronchogenic carcinoma that is caused by smoking. There are no known racial and ethnic considerations.

Nitric oxide synthase and reproductive ageing

An alternative hypothesis is that ageing is associated with an excessive synthesis of NO resulting in the accumulation of its cytotoxic metabolites such as peroxynitrite, leading to neuronal apoptosis. The process might affect the hypothalamic neurons including those that secrete GnRH. Such cytotoxic effects of excessive levels of NO could result in accelerated apoptosis of other components of the reproductive axis such as the testes. The high NO levels in tissues of ageing animals may occur as a result of excessive stimulation of nNOS by activation of NMDA receptors or the spontaneous expression of inducible NOS (iNOS), the NOS isoform that is induced during autoimmunity, inflammation and degeneration. In normal physiological conditions iNOS is undetectable in the organs of adult laboratory animals and is expressed in high levels only after exogenous cytokine stimulation and in inflammatory or infectious processes. To study the role of NOS in reproductive ageing, our laboratories...

Innate Regulators of Autoreactive T Cell Priming

During the last few years, so-called danger signals have been characterized molecularly. They, amongst others, include bacterial and viral oligonu-cleotides, bacterial and fungal cell wall components such as lipopolysaccha-rides (LPS), or bacterial proteins derived from flagellae 25, 26 . They all have in common that they are ligands for specific pattern-recognition receptors called toll-like receptors (TLRs) on innate antigen-presenting cells 25 . The TLR family is built of ten members, each specifically recognizing a different pattern. For example, TLR4 recognizes LPS and TLR9 is engaged by DNA oligonucleotides. Intracellular TLR signaling involves different adaptor molecules such as MyD88 or TRIF and commonly results in the activation of the transcription factor NF-kappa B 27 . Consequences of toll-like receptor triggering are the release of interferons and other cytokines as well as the expression of co-stimulatory molecules. In an autoimmune myocarditis model, only...

Regulatory T Cells and Their Relation to Toll Like Receptor Signals

Another control mechanism of autoreactive T cell priming has been proposed to be mediated by so-called naturally arising regulatory T cells. These T cells develop in the thymus, are mostly but not exclusively CD25+, and are functionally characterized by expression of the transcription factor FoxP3 41,42 . Upon T cell receptor triggering, so-called T regulatory cells seem to suppress the activation of CD4+ and CD8+ T cells both in vitro and in vivo assays. The mechanism of suppression is still debated but seems to be partly contact-dependent, although cytokines such as IL-10, IL-4, and TGFp may play an additional important role. The contact-dependent suppression involves CTLA4, whose expression is tightly regulated by FoxP3 41 . Recent evidence has revealed that regulatory T cells paradoxically require the cytokine IL-2, which was known for some time to accelerate T cell activation 43,44 . Together with the fact that CD25 functions as an IL-2 receptor chain, it might be suggested that...

Prevention and Control of Human Polymavirus Infections

The most serious polyomavirus infection in humans, PML, is caused by JCV. There is no proven treatment for this disease, and the prognosis for PML patients has generally been poor. If some degree of success in therapy is to be achieved, top priorities must include attempts to make an early diagnosis, to shore up the host immune response and to inhibit viral multiplication with antiviral agents. Although sporadic success has been reported using antiviral agents such as nucleic acid base analogs (e.g. cytosine arabinoside Ara-C ) and interferon, a recent study conducted under the auspices of the NIH Neurological AIDS Research Consortium failed to demonstrate significant clinical benefit for patients receiving Ara-C therapy. Given that PML nearly always occurs in severely immunocompromised individuals, there are two groups of patients for which an effective strategy is being developed. Individuals undergoing immunosuppressive therapy to control autoimmune disease or to prevent allograph...

Downregulation Occurs Within Dendritic Cell Clusters

Regulatory clusters of cells within the immune system probably play an important part in regulating autoimmunity, as is argued from the studies listed in Table 3. Each dendritic cell (DC) located within lymph node or spleen, together with the cluster of T cells that forms around it, comprises an autonomous regulatory unit. Within the cluster, signals pass between the DC and its surrounding T cells via the immunological synapse. Cytokines signal between all cell types in the cluster (paracrine activity), but at normal levels of activity each cluster forms an autonomous unit with little endocrine transmission of signals between clusters. T cells within a cluster signal to one another not only via cytokines but also via the DC itself (Tada's term epicrine activity applies). As shown in Fig. 2, each cluster operates as a democracy in which the outcome is determined by voting among its constituent cells according Autoimmune disease Fig. 2 Majority rule in the autonomous T cell cluster. The...

Overview of Cytokine Networks

With further development of the virus-specific immune response, CD4+ T cells tend to differentiate into different types of T-helper (Th) cells. Type 1 CD4+ T (Th1) cells develop under the influence of IFN-g and produce primarily IFN-g and TNF-b (LT-a) and are associated with classic delayed type hypersensitivity or cellular immune responses. Type 2 CD4+ T cells develop under the influence of IL-4 and produce primarily IL-4, IL-5, and IL-13 and are associated with strong antibody responses to viral antigens. A third type of CD4+ effector cells (Th17) develop under the influence of transforming growth factor (TGF)-b and produce IL-17 and IL-6 and are associated with inflammation and autoimmune disease. Cytokines produced by CD4+ T cells are necessary for B-cell development and for the switch from B cells producing IgM to B cells producing more mature forms of immunoglobulin such as IgG, IgA, and IgE and for B cell maturation into long-lived antibody-secreting cells. Both CD4+ and CD8+...

Childhood Hyperthyroidism

Central to considering the use of radioactive iodine and other treatment options in Graves disease in the pediatric population, is recognition of the natural history of the autoimmune disorder. One must also consider how long antithyroid drug therapy should be continued before moving on to definitive therapy.

Various Molecules Are Involved in the Clearance of Dying Cells

One major eat me signal for phagocytes on both apoptotic and necrotic cells is the exposure of phosphatidylserine (PS) 28 . Many receptors and adaptor molecules have been shown to contribute to the recognition and uptake of apoptotic cells by phagocytes (reviewed in 59 ) collectin receptors, calreti-culin CD91, Fcy-receptors, c-Mer, the p2-glycoprotein-1-receptor, integrins, lectins, CD14, the putative PS-receptor, ABC transporters, and scavenger receptors including CD36. Most of these receptors do not directly bind to apoptotic cells, rather the dying cells are engaged via bridging molecules (reviewed in 25 ). Normally, apoptotic cells are efficiently taken up by phagocytes in the early phase of apoptosis. Defects in important recognition molecules for apoptotic cells can lead to autoimmunity 25 . Impaired clearance of apoptotic cell material or increased apoptosis has been implicated in the pathogene-sis of systemic lupus erythematosus (SLE) 27,38,43 . Several gene-targeted mice...

Treatment Approaches for Children

Based on what is now known about the risks and benefits of different treatments and the pathogenesis of Graves' disease, we can now be more selective in our approach to therapy. To reduce treatment risks and expedite cures, the treatment of the child or adolescent with Graves' disease can be guided by the patient's age and the nature of the intrinsic autoimmune disease.

Discharge And Home Healthcare Guidelines

646 Myasthenia Gravis Myasthenia Gravis yasthenia gravis (MG) is an autoimmune disease that produces fatigue and voluntary muscle weakness, both of which become worse with exercise and improve with rest. The muscles that are frequently involved include those for eye and eyelid movement, chewing and swallowing, breathing, and movement of the distal muscles of the extremities. This weakness progressively worsens during the day or at times of stress, so the greatest fatigue is likely to occur at the end of the day. MG frequently accompanies disorders of the immune system or the thyroid gland. MG, thought to be an autoimmune disorder, is caused by a loss of acetylcholine (ACh) receptors in the postsynaptic neurons at the neuromuscular junction. About 80 of all MG patients have elevated titers for ACh receptor antibodies, which can prevent the ACh molecule from binding to these receptor sites or can cause damage to them. MG is often associated with thymic tumors. There appears to be...

AID haploinsufficiency

Bcl-xL transgenic AID+ - mice developed tumors after pristane treatment, their incidence was significantly reduced when compared to their AID wild-type counterparts (Takizawa et al., 2008). In addition, AID+ - mice exhibit a delayed production of high affinity antibodies against pathogens and in the development of autoimmune disease in a lupus prone model (Jiang et al., 2007 Jiang et al., 2009). These latter findings highlight the relevance of AID gene dose for B cell neoplasia generation and autoimmune susceptibility in vivo. Together these results indicate that physiological AID expression levels are limiting for its function, probably allowing an efficient diversification of antibodies while preventing unwanted DNA lesions. However, the interplay between this and other AID regulatory mechanisms can be unexpectedly complex.

Clinical manifestation

Musculoskeletal system arthralgias and morning stiffness sometimes mimicking other systemic autoimmune diseases hand and joint function may decline from skin tightening acroosteolysis (i.e., resorption or dissolution of the distal end of the phalanx) sometimes occurs flexion contractures

Postthymic Tcell Deletion

T cells that bind with high affinity to self-derived peptides presented on MHC molecules in the thymus are deleted from the repertoire. Not all self antigens are expressed in the thymus, and so mechanisms must exist for refining the repertoire of mature T cells that the thymus exports. How this is done is not fully established. It is known that antigens must be presented correctly to T cells. That means that not only must there be binding between the TCR and its cognate MHC-peptide combination, but several accessory binding events must also take place between the T cell and the antigen-presenting cell. Few normal cells bear all the necessary accessory ligands, which are found primarily on dendritic cells and cells of the macrophage family. Thus, a T cell that happens to bind to a self antigen on, for instance, a kidney cell, will find itself receiving some, but not all, of the necessary activating signals. T cells seem to interpret this incomplete signal as dangerous, and cease to...

Neuromuscular and Cutaneous Syndromes

The idiopathic inflammatory myopathies are systemic autoimmune diseases characterized by chronic inflammation leading to progressive weakness of the proximal muscles. In 7 - 66 of cases of adult dermatomyositis, different malignant tumors can promote the difficult cascade mechanisms at the cell level, leading to rapid weakness of skeletal muscles (Mooney et al. 2006). A case with all characteristic signs of acute, se-

Proinflammatory Cytokine Profiles In

IL-6 is a pleiotropic cytokine known to regulate hematopoiesis and contribute significantly to inflammation and immune responses 1 . Although it has been implicated in numerous autoimmune diseases, its role in MS was first suggested by several studies describing its upregulation in the blood, cerebrospinal fluid (CSF), and brain tissue of MS patients 2 . More recently, microarray analysis from MS lesions revealed that the nuclear factor that mediates IL-6 transcription (NF-IL6) was highly upregulated in all the MS samples examined 3 . In EAE, IL-6 gene expression is also markedly upregulated in CNS tissue and correlates well with clinical severity 4 . TNF-a is a prototypic inflammatory cytokine long implicated in autoimmune diseases. It is strongly produced by activated macrophages but is also expressed by T cells, NK cells, mast cells, endothelial cells, fibroblasts, microglia, and astrocytes 11,12 . TNF-a is produced in two biologically active forms, a transmembrane protein and a...

Staphylococcal Enterotoxins

In addition to their nature as superantigens, SEs function as potent gastrointestinal toxins causing SFP, which has a major public health impact. 1,3-5 Superantigenicity and emesis activities of SEs have been shown to result from distinct regions of the toxin protein. SEs comprise a family of homologous but antigenically different exotox-ins, which are heat stable and resistant to inactivation by gastrointestinal proteases. SEs have also been implicated in several allergic and autoimmune diseases. The repertoire of SEs includes the five classical enterotoxins SEA through SEE and the more recently identified enterotoxins starting with SEG (Table 1). To date, the ''alphabet'' of SEs and their coding genes has reached the letter ''Q.'' However, some of the recently described SEs were shown to be nonemetic, thus actually lacking the defining property of SEs. Nevertheless, the standard convention hitherto has been to refer to proteins exhibiting sequence similarity to SEs as enterotoxins.

From Genes to Disease The Basic Science Approach

The weakness of the basic science approach is the difficulties to clearly define the pathology of the phenomenon. In search of the pathologic effect of the mechanisms, numerous experiments has been carried out in animal models for human diseases where basically any disturbance of the physiology after knocking out a hypothesized gene is described as pathological. Clearly, in a complex system such as the immune system, the result will be pathologic in most cases, but the question remains, what is relevant for a naturally selected disease as occurring in humans And how do we know that the postulated genes, proteins, mechanisms, or pathways are indeed relevant and essential for an autoimmune disease in humans One way to find out is to first identify the genes involved in the disease development. Then, when we have defined the most critical genes and thereby the most critical pathways, the basic approaches to studying the molecular interacting pathways will be crucial for understanding the...

From Disease to Genes The Monogenic Success and the Polygenic Failure

The cause of autoimmune diseases seems to be easily delivered by genetics. Why not just define the genes carried by diseased individuals and then determine their functional genetics Is this not just a question of adding resources into the human genetic project and its prolongations in the form of various strategic research platforms The human genome project has indeed been fruitful and we have had enormous success with hundreds of monogenic diseases. One example in the autoimmune field is the identification of the AIRE (autoimmune regulator) gene causing the APECED syndrome 9, 10 . The APECED syndrome is a familiar disease characterized by a combination of fungal infections and autoimmune inflammation of various endocrine organs. It is a monogenic disease with high penetrance and caused by mutations in the AIRE gene. This discovery did not only identify the gene behind APECED but also led to a renewed understanding of autoimmunity as the AIRE gene plays an important role in the...

The Use of Animal Models in a Diseaseto Gene Approach

Experience from studies on animal models of autoimmune diseases show that they are much more efficient and appropriate for linkage analysis than human cohorts. The process of positional cloning involves five generic steps that intend to lead from phenotype to gene discovery (described in Fig. 2). In general, an F2 intercross of 100-400 animals will reveal loci explaining 10 -50 of a given disease trait and also allows for studying some of the genetic interactions involved. Thus, the power is much higher compared to human studies. What we have learned from animal models for autoimmune diseases so far is that there are a multitude of genes of variable penetrance controlling a disease, and in addition, there are complex genetic interactions and also interactions with the environment. It is important to remember that, depending on the phenotype, the number of loci, their relative effects, and how they interact with each other and the environment varies considerably. Most likely, the...

Urinary frequency and urgency

Cystitis Symptoms Women

Interstitial cystitis produces severe symptoms which include frequency, dysuria, lower abdominal and urethral pain. It affects individuals of both sexes although only about 10 of sufferers are men. Although the peak age is 30-50 years 261 it has also been found in children 262 . The aetiology remains obscure but the absence of any detectable bacterial or fungal agent is a prerequisite for the diagnosis 263 . There is growing evidence that interstitial cystitis is an autoimmune disease. Histologi-cal changes in bladder wall biopsies are consistent with a connective tissue disorder. The most common marker is mast cell infiltration of the muscularis layer of the bladder. This was first recognized in 1958 by Simmons and Bruce and, although there is no consensus on the role of mast cells and their usefulness as a diagnostic criterion, two papers have investigated degranulation of mast cells 264, 265 both showing increased degranulation in patients

Management of secondary amenorrhoea

Overall, the most common cause of POF is autoimmune disease with infection, previous surgery, chemo- and radiotherapy also contributing ovarian autoantibodies can be measured and have been found in up to 69 of cases of POF. However, the assay is expensive and not readily available in most units. It is therefore important to consider other autoimmune disorders, and screen for autoantibod-ies to the thyroid gland, gastric mucosa parietal cells and adrenal gland if there is any clinical indication.

Antiinflammatory Cytokine Profiles In

During the course of CNS autoimmunity, IL-10 can be produced by macrophages, Th2 cells, B cells and DCs, in addition to astrocytes and microglia 19,53,119,120 . IL-10 has well-documented inhibitory effects on Th1 proliferation and effector cytokine production and is also a potent inhibitor of APC function through its ability to decrease MHC Class II and B7 expression and proinflammatory cytokine and chemokine production 121-123 . In contrast, IL-10 is also known to promote B cell differentiation, survival, and immunoglobulin production class switching and induce CD8+ T cell proliferation and cytotoxic activity. Based on these potent immunomodulatory functions, IL-10 has been investigated as an anti-inflammatory mediator in both EAE and MS. Some of the earliest studies examining the role of endogenous IL-10 during autoimmunity reported decreased IL-10 mRNA expression coincident with disease remission in both the mouse and rat EAE systems, and a similar decrease in IL-10 mRNA expression...

Evaluation of Eyelid Malpositions

Basal Cell Carcinoma Eyelid

A history of slow progression is not uncommon with most involutional eyelid changes, but this usually occurs over several years. Almost all patients with ptosis or dermatochalasis will report some increase in droopiness late in the day or when tired this does not usually indicate myasthenia gravis. The occurrence of an eyelid malposition with orbital pain is always worrisome and demands investigation to rule out neoplasm or pseudotumor. Any such association requires radiographic study. Any patient with a history of significant worsening of ptosis late in the day or when tired should be suspected of having myasthenia gravis. This is especially true if the eyelid appears near normal in the morning, or the condition is associated with difficulty in swallowing, generalized weakness, or diplopia. A levator fatigue test can be performed easily without risk. The patient is asked to look upward for several minute without blinking. The position of the eyelid is measured before and immediately...

Frequency and timing of antenatal visits

Conditions such as hypertension, cardiac or renal disease, endocrine, psychiatric or haematological disorders, epilepsy, diabetes, autoimmune disease, cancer or HIV Factors that make the woman vulnerable such as those who lack social support Age 40 years and older or 18 years and younger BMI greater than or equal to 35 or less than 18 Previous Caesarean section Severe pre-eclampsia or eclampsia Previous pre-eclampsia or eclampsia Three or more miscarriages Previous preterm birth or midtrimester loss Previous psychiatric illness or puerperal psychosis Previous neonatal or stillbirth Previous baby with congenital anomaly

Natural Antibodies To Cytokines

Natural Ab against IFN in humans were first reported in 1981 as a case of neutralizing IFN-a Ab in a patient with varicella-zoster (13). Later, IFN-a Ab were found in patients with other viral infections, with neoplastic and autoimmune diseases, and in a patient with chronic graft versus host disease (6,7,13-24). The prevalence of IgG anti-IFN-a Ab in these patients is about 10 .

AIDdeficient autoimmuneprone mice

This is the first model combining autoimmunity with AID-deficiency. MRL lpr mice develop a lupus-like syndrome that shares many similarities with human SLE such as high levels of circulating autoantibodies, particularly to double-stranded DNA (dsDNA), deposition of immune complexes, particularly in the kidneys, and glomerulonephritis (Theofilopoulos and Dixon, 1985). When AID-deficient, these mice experience a highly significant decrease in kidney damage, and a dramatic increase in survival to levels that exceeded even mice lacking secreted antibodies, suggesting that improved survival did not result just from the lack of pathogenic IgG antibodies but that other factors also contributed. The proportion of activated autoreactive T cells were unchanged suggesting that the increase in survival did not come from the antibody-independent role of B cells in autoimmunity. These mice have very high levels of autoreactive IgM, not only demonstrating that autoreactive IgM...

Thyroid Disease in Turner Syndrome

Many authors reported on a higher prevalence of hypothyroidism and an association with positive thyroid antibodies in TS patients (table 2) 2, 6, 7, 24, 29, 32, 37 . Hypothyroidism is found in up to 35 of TS patients. Thyroid autoimmunity seems to be even more common in females with Turner syndrome with a prevalence of up to 52 15 . A positive family history was reported by Wilson et al. 37 . This group found an increased incidence of thyroid antibodies in patients with TS and their first degree relatives. The incidence of thyroid antibodies was 30 in patients compared to 1.7 in an age matched control group and 22 in the mothers of the TS patients (vs. 6.6 in the controls). Larissa et al. 21 found a preferential parental segregation of autoimmunity in their study. There is no clear explanation for the higher frequency of thyroid auto-immunity in Turner syndrome. The positive family history could give a link to genetic co-etiology. HLA association is discussed very controversially in...

Expression of FRs in Normal Tissues

FRs have also been detected in normal tissues, particularly those involved in the retention and uptake of the vitamin. For example, the choroid plexus in the brain expresses high levels of FR. However, the receptor is primarily localized to the brain side of the blood-brain barrier, where it is inaccessible to blood-borne folates or folate-drug conjugates.59,65,66 The FR has similarly been located on the apical membrane surface of the intestinal brush border,67 but again, access to these docking sites requires either escape into the lumen of the intestine or oral ingestion of the folates. FR is also expressed at high levels in the proximal tubules of the kidney, where it is believed to capture folates (and small molecular weight folate-drug conjugates) prior to their urinary excretion and then return them back into circulation via a transcellular reabsorption process.68-70 Recent reports further reveal FR expression on activated but not resting macrophages,71,72 an observation that...

Therapies For Microvascular Insufficiency

Peripheral Vasodilation

Protein kinase C (PKC) and diacylglycerol (DAG) are intracellular signaling molecules that regulate vasculature by endothelial permeability and vasodilation. The PKC isozymes are a family of 12 related serine threonine kinases (25) whose normal function is the activation of essential proteins and lipids in cells essential for cell survival. PKC-P is expressed in the vasculature (26,27) and belived to be involved in cell proliferation, differentiation, and apoptosis. PKC is activated by oxidative and osmolar stress, both of which are a consequence of the dysmetabolism of diabetes. Increased polyol pathway activity and pro-oxidants bind to the catalytic domain of PKC and it is disin-hibited. PKC-P overactivation is induced by hyperglycemia or fatty acids through receptor-mediated activation by phospholipase C. It is hypothesized that AGEs and oxidants produced by nonenzymatic glycation and the polyol pathway, respectively, increase the production of DAG (28). Increased DAG and calcium...

Potential Complementbased Therapeutics

The development of complement inhibitors that can be used in vivo, while still in the developmental stages is rapidly accelerating119. Acute injury inflammation is much more amenable to complement inhibition, since the drug need only be administered transiently120,121, whereas inhibition of complement for chronic disorders for longer periods of time may generally lead to susceptibility to infection and or autoimmunity. However, Bergamaschini et al. administered Enoxaparin, a low-molecular-weight heparin, to the APP23 transgenic mouse three times a week for 6 months. This compound, which had no noted toxicity and was demonstrated to inhibit AB-induced complement and contact system activation and amyloid-induced toxicity of differentiated PC-12 cells, demonstrated a greater than 2-fold decrease in amyloid deposits, total amyloid load, and decreased astrogliosis122, similar to the reduction reported by Fonseca et al. in C1q-deficient animals. Compstatin is perhaps the most promising...

Thyroid Disease in Diabetes Mellitus

The most frequent autoimmune disease in type 1 diabetes affects the thyroid. The etiology of autoimmunity in pancreas and thyroid is a T cell-mediated disease and seems to be due to common genetic susceptibility. Two immune regulatory genes (HLA human leukocyte antigen and CTLA-4 cytotoxic T lymphocyte-associated protein 4) contribute to the susceptibility for both diseases 5, 23 . This locus, also known as the IDDM 12 gene, seems to play a major role in development of autoimmune polyglandular syndrome type 2 (APS-2).

Micronutrients and Microparticles

Both in food and water supply, metals and minerals, as well as other microparticles, are abundant, and as such more common as part of pollution in industrialized areas. These particles may act in different ways with the immune system, causing primary or secondary effects. It has been suggested that exposure to xenobiotic-like metals may induce immune responses in autoimmune diseases. Such reactions have been related to effects of mercury 105 , cobalt, zirconium, beryllium, silver, and aluminum 54 , Especially aluminum is ubiquitous in the Western culture and represents the most widely used trace element in food, water, soil, and pharmaceutical agents. Moreover, food additives and processed foods, such as cheese, baked goods, grain products, cake, and pancake mixes, vending machine powdery, milk, cream powder substitute, and soy-based milk formulae, sugar and frozen dough, add substantial amount to Al intake. Additionally, different substances, when added to water and even water...

Current Clinical Neurology

Vitek, and Andres M. Lozano, 2003 Myasthenia Gravis and Related Disorders, edited by Henry J. Kaminski, 2003 Seizures Medical Causes and Management, edited by Norman Delanty, 2002 Clinical Evaluation and Management of Spasticity, edited by David A. Gelber and Douglas R. Jeffery, 2002

Gastroduodenal Dysfunction The Gastroparesis Syndrome

Endoneurial Blood Flow

Another possible connection between diabetes mellitus and the GI tract can be infrequent autoimmune disease associated with type 1 diabetes mellitus, such as celiac disease, autoimmune chronic pancreatitis, and autoimmune gastropathy (2). Indeed, about 15-20 of patients with type 1 diabetes mellitus exhibit parietal cell antibodies (26), but on the other hand no clear-cut relationship has been found between parietal cell antibody titers and delayed gastric emptying (26). Finally, the finding of gastroparesis associated with autonomic neuropathy in a diabetic should not preclude the possibility of coexistent mechanical factors contributing to the apparent motor abnormality (27). First assessing the possibility of mechanical obstruction remains a key premise to diagnosing a gut motor disorder under any circumstances.

The Alternative Pathway of Complement a Pattern Recognition System

Diy Porch Swing Plans Free Templates

Based on the toxic activity of the activated complement system the individual reactions of the cascade are tightly balanced and activation must be focused to the surface of the foreign invader. At the same time adjacent, neighbouring self cells, i.e. bystander cells must be protected. Thus for the host activation and effector function is desired on the surface of a microbe but simultaneously the same reactions must be inhibited on the surface of any host cells, particularly those cells that are located in direct vicinity of the microbe. Consequently host cells must actively downregulate the immune response and the inflammatory reactions. The limitation in terms of time and space is a central aspect of the immune response and of inflammatory reactions, and inappropriate control results in autoimmunity. The recent research has highlighted the central role of the innate immunity (Medzhitov and Janeway 1997). The innate immune system acts independently, but also in combination with the...

The Acute Phase Response and Alzheimer Disease

The acute phase response (APR) is an orchestrated physiological response of the body to tissue injury, infection, or inflammation. A prominent feature of the APR is the induction of acute phase proteins, which are involved in the restoration of homeostasis. Cytokines including interleukin-1 (IL-1), IL-6 and tumor necrosis factor-alpha (TNF-a) are important mediators of the APR. Different signaling pathways are activated by different cytokine-recep-tor interactions. Eventually, cytokine-inducible transcription factors interact with their response elements in the promoter region of acute phase genes and their transcription is induced (or inhibited). The APR also involves activation of the hypothalamic-pituitary-adrenal (HPA) axis. Examples of serum proteins whose levels increase in a systemic APR are a1-ACT, amyloids A and P, and ferritin (the major iron storage protein). Serum amyloid A is an acute phase protein that modulates proteoglycan synthesis in cultured murine macrophages...

Rapid ACTH Stimulation Test

Bances to rule out pituitary or hypothalamic tumor. X-rays are generally not useful in patients with primary adrenal insufficiency caused by autoimmune disease. In all other cases, a CT of the abdomen may reveal enlarged adrenal glands, which may need to be biopsied by CT-guided fine needle for the diagnosis.

The Injectable Bulking Agents

The particle size generally falls within the 100- to 450- m range, but there are smaller particles within the gel. Potential for migration of smaller particles has been suggested, and this could potentially lead to the possibility of granuloma formation. However, animal studies have shown minimal local reaction and a lack of distal migration. There have also been concerns about a possible link between silicone and autoimmune disease, but again, recent data appear to refute this. One disadvantage of this product is its high viscosity, which makes it difficult to inject, with difficulty increasing with needle length. A specially designed gun is supplied for injection into the anal canal, and the agent's smooth deployment may improve with experience.

The Cognate Immune Response

Probably the best studied model of T-cell-mediated autoimmune disease is experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis in humans. This disease is critically dependent on antigen-specific CD4+ Th1 cells that produce IFN-y, because it can be adoptively transferred by these cells into a na ve host. Antigen-specific CD4+ T-cells that have a Th2 phenotype and produce IL-4 do not cause disease and, under some circumstances, can be protective. The ob ob mice are totally resistant to induction of EAE but develop disease to the same extent as wild-type mice when given leptin exogenously (118). This disease protection is caused by skewing of the immune response toward a Th2 phenotype. When leptin is given to ob ob mice, Th1 CD4+ T-cells are generated normally and produce similar amounts of IFN-y in vitro to wild-type mice. Associated with this is impaired antibody isotype switching. In untreated ob ob mice, all of the antigen-specific antibody produced in...

Ficolins and Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease with of unknown cause, but immune dysfunction is clearly one of its central features. H-ficolin was firstly identified as a serum antigen target for an autoantibody present in the sera of some patients with SLE. That might participate in the pathogenesis of SLE. Anti-H-ficolin antibody appears during the active hypocomplementemic phase in some SLE patients and its concentration was found to correlate positively with diseases activity in SLE (Yoshizawa et al. 1997).

Strength of BCR signal

Fig. 3 Basic mechanisms known to be involved in the prevention of B cell autore-activity and dependent on the BCR signal strength. A further mechanism known as receptor revision editing may also prevent autoimmunity but apparently is not strictly dependent on the BCR signal munization of bcl-2-transgenic mice resulted in 20-fold more memory B cells than controls. Furthermore, a high proportion of these bcl-2-transgenic memory B cells, despite having a typical memory phenotype, retained their VH genes in a low-affinity configuration. Thus, these memory B cells showed no evidence of having undergone affinity maturation, as the low-affinity B cells would have been expected to lose the competition for antigen in the GC and die by apoptosis. An additional bcl-xL transgenic mouse also preserved low-affinity cells in the GC, although in this case the low-affinity cells were not germline variants of the dominant clonotype, but rather were B cells using VH genes that usually appear only during...

Primary Nursing Diagnosis

Assist the patient in working through any feelings of depression that can occur because of MG's profound effect on lifestyle, roles, and responsibilities. Depression can also result from the disbelief by others of the MG diagnosis because the patient may appear to have suspiciously fluctuating symptoms. Provide encouragement to these patients to live full, productive lives. Educate the family and significant others on the fluctuation of MG, and place them in contact with support groups and the Myasthenia Gravis Foundation.

Brain Autoantigens in the Immune System

Myelin basic protein (MBP) is the classical brain-specific autoantigen. In many species and strains of animals, immunization against MBP in suitable immune adjuvants almost unfailingly results in the development of experimental autoimmune encephalomyelitis (EAE), a T cell-mediated autoimmune disease targeted exclusively against CNS white matter. The exquisite tissue specificity has been traditionally explained by a correspondingly restricted tissue distribution. Indeed, MBP is produced at the highest level in CNS myelin sheaths, where it is positioned on the inner membrane leaflets, not on the surface (Campagnoni and Macklin 1988). EAE, experimental autoimmune encephalomyelitis EAMG, experimental autoimmune myasthenia gravis T1D, Type-1 diabetes mellitus EAU, experimental autoimmune uveitis EAT experimental autoimmune thyroiditis EAE, experimental autoimmune encephalomyelitis EAMG, experimental autoimmune myasthenia gravis T1D, Type-1 diabetes mellitus EAU, experimental autoimmune...

Tertiary prevention of hypothyroidism Avoiding Complications

Although autoimmune thyroiditis is not a complication of hypothyroidism per se, patients affected with it are also at risk of developing a relatively small set of associated autoimmune disorders. The polyglandular autoimmune syndrome type II includes hypothyroidism, primary adrenal insufficiency, and type I diabetes (57). Less commonly, hypothyroidism may occur in the autoimmune dystrophy syndrome (or polyglan-dular autoimmune syndrome type I). Autoimmune thyroid disorders are associated with increased risk of developing pernicious anemia and gastric achlorhydria caused by intrinsic factor and parietal cell autoimmunity. Patients with autoimmune thyroiditis should be monitored for vitamin B12 deficiency with periodic complete blood counts and, whenever the disorder is seriously suspected, serum vitamin B12 measurement. Vitiligo, leukotrichia (prematurely gray hair), and alopecia areata have also been associated with autoimmune thyroiditis although these disorders are often...

Monitoring of the Fetus in a Mother with Graves Disease

In areas of iodine deficiency the circulating maternal thyroxine concentrations are low although TSH is usually in the normal range. In this situation the incidence of thyroid abnormalities is higher and in particular thyroid autoimmunity may be associated with diminished thyroid reserve and an increase in spontaneous abortion.

Effects on Particular Organs or Organ Systems

Immune System The immune system consists of various organs, including the bone marrow, spleen, thymus, and lymph nodes, plus specialized cells and plasma proteins produced by those organs which circulate in the blood and lymphatic system. The cells are the lymphocytes, or white blood cells, and include T cells and B cells. The proteins include the immunoglobulins, interleukins, and the complement system. Together they act to rid the body of chemical and biological contaminants. There are three types of immune system derangements. Immunosuppressants reduce immune response and render the body more vulnerable to foreign substances. Immunostimulants cause hypersensitivity reactions or allergies. Autoimmune disease is the condition where the immune system attacks its own substances as if they were foreign. Immunostimulants usually cause their reaction within 15 minutes of exposure. A first exposure does not cause a reaction since the immune system must generate immunoglo-bulin antibodies....

Activation of Ignorant Autoreactive T Cells The Transition from Autoreactive to Autoaggressive

Now that it is clear that the immune repertoire contains millions of potentially autoreactive T (and B) lymphocyte clones, one may certainly wonder why so few people (and animals) actually develop autoimmune disease. The answer is that autoreactive T cells are not automatically pathogenic, i.e., autoaggressive. In order to become able to attack their autologous target tissues, an autore-active T cell must be activated. But activation is not easy to achieve, since there seem to be several tiers of regulatory controls that safeguard the non-pathogenic status of the autoreactive T cells. Breakage of these controls seems to occur only under very special circumstances, as is the case with immunization of animals with autoantigens in complete Freund's adjuvant. Traditional concepts list four activation mechanisms that may break tissue-specific autoimmunity, most of these related to concurrent microbial immune responses. These are Historically, molecular mimicry was the first, and over a...

Primary Adrenal Insufficiency Addisons Disease

Suncongentcral Hemorrhage

Primary adrenocorticol insufficiency results from any disease process (Table 1) that damages the entire adrenal cortex, thus resulting in deficiencies of cortisol, aldosterone, and adrenal androgens. Approximately 75-80 of cases are owing to autoimmune adrenalitis (5), a shift from the predominant cause in 1928-1938, which was tuberculous adrenalitis (now only accounting for 10-20 worldwide). Although circulating antibodies to adrenal antigens, predominately 21-hydroxylase (6), are found in 70 of patients, their role in the etiology is not clear, although they may be present years before the clinical diagnosis. It is recommended that adults and children with other organ-specific autoimmune disease (see below) particularly hypoparathyroidism and type 1 diabetes, be screened for the presence of 21-hydroxylase autoantibody if this is positive, such patients should be screened for adrenal function every 6 mo (7).

Retraction of the Eyelid

INTRODUCTION Eyelid retraction may be seen as a sequel to trauma, surgery, or orbital disease. The most common cause is Graves' disease. This is a systemic autoimmune disease in which the primary target of the immune response is directed toward the TSH receptor of the thyrocyte. Extrathyroidal manifestations principally involve specific fibroblasts of the orbit and of the pretibial dermis. The immune reaction is mediated by anti-TSHR T-cells and results in the release of a Th-1 cytokine profile, proinflammatory mediators, and growth factors that cause deposition of glycosaminoglycans, adipose proliferation, and collagen synthesis with chronic fibrosis. Through the phenomenon of epitope spreading, adjacent tissues become involved, including the extraocular and eyelid muscles, and connective tissue sheaths and fascia.

Autoantibodies in diabetes complications

The lack of an immune response to self when responses to environmental antigens are retained is due to immunological tolerance. The role of tolerance, or lack of tolerance, is important to the understanding of autoimmune diseases and transplantation immunobiology (Mackay 2000). A loss of natural tolerance (to self) underlies all autoimmune diseases. Many more individuals develop autoimmune phenomena than autoimmune disease. Immune-mediated (Type I) diabetes results from an organ-specific autoimmune-mediated loss of insulin-secreting P cells. This chronic destruction process involves both cellular and hormonal components detectable in the peripheral blood, months or even years, before the onset of clinical diabetes (Kukreja & Maclaren 1999). In order to elicit an immune response, a molecule must be recognized as non-self by the biological system.

Fecal Incontinence in Myopathies

Dysfunction of the smooth muscles at several levels of the gastrointestinal tract in myasthenia gravis is well known, and about 33 of patients complain of significant fatigable dysphagia 95, 96 . Mastication and swallowing difficulties worsen as a meal progresses, in particular at the end of the day. Myasthe-nia gravis can also present with a clinical picture of fecal and urinary incontinence 97 .

Inappropriately applied laboratorybased tests

It has been suggested that food immune complexes may play a role in those who claim a delayed ( 2 hours) adverse response to foods. These are able to be detected using solid phase radioimmunoassay. Even within autoimmune diseases that rely on their presence as diagnostic, their role is unclear. Their clinical relevance is doubtful for two further reasons. They have not been

Biology Of Microglia

Ifn Tlr3 Cxcl10

These areas are concentrated around the subven-tricular zones where active neurogenesis occurs. These ameboid tissue macrophages then migrate throughout the entire brain parenchyma and differentiate into resident microglial cells. In the mature CNS, microglia are ubiquitously present as highly ramified cells ( resting microglia) 5,6 . They respond to changes in the CNS microenvironment in a variety of disorders with or without the participation of the systemic monocytes. Although in degenerative disorders such as AD and Parkinson's disease there is little evidence to support recruitment of monocytes from the periphery, in infectious and autoimmune diseases such as HIVE and multiple sclerosis (MS) and in stroke, there is frank infiltration of monocyte-derived macrophages as well as other inflammatory cells. Even in these diseases in which monocytes are known to contribute significantly to the disease process, studies using sensitive markers of...

Immune Theory of Aging

Original immunologic theory of aging suggests that aging in mammals is a self-destructive process leading to a decline in immune response. The failure in immune homeostasis is associated with a consequent rise in autoimmunity (Walford, 1987). Age-related phenomena such as increased prevalence of autoantibodies and monoclonal immunoglobulins reflect dysregulation of the senescent immune system rather than a simple decline in responsiveness. The age-related changes primarily occur in the T-cell-dependent immune system and are associated with increased susceptibility to infections and incidence of autoimmune phenomena in the elderly. One of the characteristics of all somatic cells is a finite life-span. Cells may proliferate until they reach a point, after which they can no longer produce daughter cells. This observation is central to the clonal exhaustion hypothesis, a mechanism cited to explain age-associated immune dysfunction. In this hypothesis, repeated division of lymphocytes...

Exercise and Immune Function

Aging leads to a diminution of resting immune function, increasing the risk of infection, tumor development, and autoimmune diseases (Shephard and Shek, 1995). The production of IL-2 is decreased, sometimes with a decrease of total T-cell count, and often with changes in T-cell subsets and proliferative responses to mitogens. However, NK cell activity remains unchanged. In theory, moderate exercise training should help to reverse the adverse effects of aging upon the immune system. However, there have been relatively few studies comparing the immune responses of young and older individuals to acute exercise and to training. A single bout of moderate exercise seems to be well tolerated by the elderly. The NK cell response is as much as in younger individuals, but perhaps because of a low initial proliferative capacity, older subjects show less stimulation of lymphocyte proliferation by moderate activity and less suppression with exhausting exercise. Perhaps because resting immune...

Acute Rheumatic Fever Introduction

Acute rheumatic fever is an autoimmune disease responsible for cardiac valve disease or rheumatic heart disease. It is associated with infections caused by the group A streptococcus and occurs about 2 to 6 weeks following a streptococcal upper respiratory infection. It is prevented by adequate treatment of the infection with appropriate antibiotic therapy within 9 days of onset of streptococcal infection before further complications can occur. Because rheumatic heart disease does not occur after only one attack and children are susceptible to recurrent attacks of rheumatic fever, it is vital that an initial episode is diagnosed and treated, and that long-term prophylactic therapy (5 years or more) is given following the acute phase. There is no specific test for rheumatic fever the diagnosis is based upon the manifestations using the revised Jones criteria as a guideline. Jones criteria consist of major manifestations (polyarthritis, carditis, chorea, subcutaneous nodules, and...

Fetal Maternal Relationships

Thyroid hormone transport proteins particularly TBG (thyroxine-binding globulin) increase due to enhanced hepatic synthesis and a reduced degradation rate due to oligosaccharide modification. Serum concentration of free thyroid hormones has been reported to be decreased, increased or unchanged during gestation by different groups depending on the assays used 9 . However, there is general consensus that there is a transient rise in free thyroxine (FT4) in the first trimester due to the relatively high circulating hCG concentration and a decrease of FT4 in the second and third trimester albeit within the normal reference range. Recently, it has become apparent that there is a need for normative trimester-specific reference ranges for thyroid hormones 10 . Ideally these should be derived from iodine sufficient women who do not have any evidence of thyroid autoimmunity 11 . Changes in free triiodothyronine (FT3) concentration are also seen in which they broadly parallel the FT4, again...

Nutrition Intervention

Fish oils are rich in the long-chain ra-3 polyunsaturated fatty acids (PUFAs), eicosapentanoic (20 5ra-3) and docosahexaenoic (22 6ra-3) acids. Linseed oil and green plant tissues are rich in the precursor fatty acid, a-linolenic acid (18 3ra-3). Most vegetable oils are rich in the ra-6 PUFA linoleic acid (18 2ra-6), the precursor of arachidonic acid (20 4ra-6). Arachidonic-acid-derived eicosanoids such as prostaglandin E2 are proinflammatory and regulate the functions of cells of the immune system. Consumption of fish oils leads to the replacement of arachidonic acid in cell membranes, diminishes lymphocyte proliferation, T-cell-mediated cytotoxicity, NK cell activity, macrophage-mediated cytotoxicity, monocyte and neutrophil chemotaxis, major histocompatibility class II expression, and antigen presentation, production of proinflammatory cytokines (IL-1, IL-6, TNF), and adhesion molecule expression. Studies on animal models indicate that fish oil reduces acute and chronic...

Potential Mechanisms

And engage T cells recognizing the particular MHC class II families (Fig. 2). Thus, populations of T cells, some of which recognize self peptides, are activated and potentially could initiate autoimmunity. For B cells (production of autoantibodies), infection by Epstein Barr virus (EBV) leads to the production of autoantibodies. B cells differentiate into plasma cells and secrete antibody of a single specificity. This can be antiviral or of antiself specificity. Normally, B cells require interleukin (IL)-2, IL-4, IL-5, IL-6 and interferon y (IFN-y) secreted by T cells for growth and differentiation into plasma cells. Infection of B cells with EBV drives these B cells to produce antibodies. Should the B cells (antibody) be specific for self protein, EBV-infected cells would produce antibodies reactive with self. Figure 2 TCR-peptide-MHC interaction. TCRs are present on the surface of T cells and are heterodimers comprising an a and a J chain. The TCR interacts with the MHC class I or...

Clinical Description

Antibodies to factor XI are rare and have mostly been described in nondeficient patients as a complication of autoimmune disease. 6 Recently, however, a number of patients who were given plasma replacement therapy were diagnosed with acquired inhibitors to factor XI. They had a mean factor XI activity level of about 1 and were all homozygous for the Glu117stop (type II) mutation, indicating that mutations associated with a very low factor XI level may be risk factors for development of an inhibitor after plasma replacement.1-11-1

Iodine Deficiency and Supplementation

Six randomized, controlled trials of iodine supplementation in pregnancy have been published, involving 450 women with mild-to-moderate iodine deficiency. In all six trials, supplementation resulted in a significant increase in maternal urinary iodine. Iodine doses varied between 50 and 230 xg day, and the data indicate no clear dose-response relationship for urinary iodine, TSH, thyroglobulin, thyroid hormone or thyroid volume. For the newborn, most data suggest supplementation is safe and efficacious. The studies also suggest an increase in newborn thyroid volume and thyroglobulin can be prevented or minimized by supplementation, which has little or no impact on newborn total or free thyroid hormone levels. There are no clinical data on the effect of supplementation on birth weight or prematurity, and no data on long-term outcomes, such as thyroid autoimmunity, or child development.

Response to Infection Host immune response

MCMV infection induces a generalized immune suppression, but enhances autoimmunity and exacerbates graft-versus-host disease. Immune suppression correlates with the mouse's genetic phenotype (susceptibility). Sublethal infection of susceptible mice reduces the number of myeloid and erythroid progenitor cells in the bone marrow, decreases leukocyte counts in the peripheral blood, and reduces (by 80-90 ) the number of thymocytes recovered from the thymus. The bone marrow atrophy and loss of cortical thymocytes is not due to lytic infection of bone marrow cells or thymocytes, but may be associated with increased maturation and migration of bone marrow cells to the sites of virus infection or Fas-mediated apoptosis (in thymocytes or bone marrow cells). Thymic involution coincides with bone marrow hypoplasia, but the two appear to be independent events. Myelosuppression is restored after treatment with the immunomodulator AS101 ammonium trichloro (dioxyethylene 0-0')tellurate ....

Prevention and Control

Despite the frequency and severity of their infection, these viruses are the least understood of the picornaviruses. The only enterovirus vaccines available at present are those against the three poliovirus serotypes. Their application for almost 40 years has resulted in the goal of eradication of poliomyelitis in the world becoming a reality. However, there are no vaccines against other enteroviruses. In view of the large number of different serotypes of echoviruses, it is difficult to design vaccines against them all. A better understanding of their genomic organization and function, as well as the mechanisms of their rapid evolution and variability, would be a great help in the design of antiviral components, where the essential functions of the virus would be a target. The studies of cell receptors are of great importance for the understanding of the interactions of a virus with its host cell, and thus the possible inhibition of virus-cell interaction. A better...

Potential Negatives Of Complement Blockade Following Stroke

It has long been accepted that complement deposition on the surface of pathogens greatly increases the rate at which these opsonized pathogens are phagocy-tosed and destroyed62. More recently, a number of studies have demonstrated that complement, particularly early components such as C1q, C3, and C4, plays a critical role in facilitating clearance of apoptotic cells62-66. Additionally, the presence of genetic complement deficiencies strongly predispose to the development of autoimmune diseases, such as lupus, which are generally considered to result in part from the failure to clear apoptotic cells62,63. It is hypothesized that apoptotic cells that are not rapidly cleared progress to lysis with release of potentially damaging intracellular substances into the surrounding extracellular tissue space67-78. Most relevantly, in cases of acute tissue injury it is likely that necrotic cell debris from uncleared apoptotic cells exacerbate the pro-inflammatory response however, this...

MBP7285 on Human Tcell Activation

Multiple sclerosis is a chronic CD4 T-cell mediated disease of the central nervous system characterized by local-cell and macrophage infiltrates, demyelination and loss of neurologic function 1,2 . MS is widely believed to be an autoimmune disease and to be triggered by CNS-specific CD4 T lymphocytes 3-6 . Candidate autoantigens include constituents of the myelin sheath such as myelin basic protein and proteolipid protein (PLP) 7 . Modem approaches towards the therapeutical management of MS involve the design and use of peptide analogues of disease-associated myelin epitopes to induce peripheral T cell tolerance 8 . Experimental autoimmune or allergic encephalomyelitis (EAE), one of the best studied experimental animal models of MS 1,9 , is a useful in vivo system for the evaluation of such therapeutic approaches. In Lewis rats immunized with guinea pig MBP protein, encephalitogenic T cells which recognise the 72-85 amino acid sequence MBP7285, dominate the immune response 10 . The...

Interleukin1 Receptor Antagonist

The allele A2 has been associated with the incidence of autoimmune diseases like lupus erythematosus and insulin-dependent diabetes mellitus (44,45). In acute systemic inflammation, there is no difference between surviving or nonsurviving patients with severe sepsis. This finding is in contrast to the results concerning the biallelic NcoI polymorphism within intron 1 of LTa Homozygotes for the TNFB2 genotype revealed a high mortality when compared to heterozygotes and TNFB1 homozygotes. The overall group of patients with severe sepsis did not show an increase in the TNFB2 allele frequency. For the IL-1ra polymorphism, however, an increase of the allele A2 in the patients with severe sepsis was detected. Patients carrying the haplotype TNFB2 homozygous and A2 homo-zygous did not survive in this study.

The Comeback of Dying Cells

About a decade ago scientists became aware that the disappearance of dead and dying cells is not just simple trash removal, and even more, that failure of removal has severe consequences and can lead to autoimmunity. The process of recognition and uptake of those cells is very complex and highly regulated. Cells can die in two main ways apoptosis and necrosis. Apoptotic cells, which maintain their membrane integrity for a certain time, have to be cleared quickly and efficiently to prevent the release of tissue-damaging intracellular constituents, which consecutively initiates inflammation. Apoptosis is viewed as programmed cell death or cellular suicide and is characterized by specific morphological changes of the dying cells, including loss of membrane asymmetry, nuclear condensation, and DNA fragmentation. Apoptotic cells are rarely to found in vivo because of their rapid and efficient clearance by professional or even amateur phagocytes.

Regulatory Suppression of Autoimmune T Cells But How Do Suppressor T Cells Know

In the case of CNS autoimmune T cells, first evidence for counter-regulatory cell loops came from early studies inoculating animals with incomplete Fre-und's adjuvant, a treatment that protected from autoimmune disease, rather than inducing it. The protective effect could not be transferred to naive recipients by serum, but by MBP-specific lymphocytes from spleen or other immune tissues (Bernard 1977 Swierkosz and Swanborg 1977). These studies marked the birth of the suppressor cell in EAE, a capricious cell that thereafter submerged for decades until its recent reappearance in a new guise, as Tregs. It seems to be safe to conclude that there are numerous distinct regulatory pathways to protect an individual from autoimmune disease. There are regulatory T cells of CD4, and of CD8 phenotype, and there are in addition NK and NK1 T cells, which may have roles in regulation (Sarantopoulos et al. 2004). The terminal act of an autoimmune disease is initiated when the autoimmune T cell...

Complement Mediated Cell Clearance

Complement deposition on the surface of pathogens greatly increases the rate at which these opsonized pathogens are phagocytosed and destroyed (Mevorach 1999). Studies have also demonstrated that early complement components such as C1q, C3, and C4 play a critical role in facilitating the clearance of apoptotic cells (Fishelson et al. 2001 Mevorach 1999, 2000, 2003 Mevorach et al. 1998). This may explain why genetic complement deficiencies strongly predispose individuals to develop autoimmune diseases, such as lupus, which are generally considered to result in part from the failure to clear apoptotic cells that spill cellular debris after acute tissue injury (Elward and Gasque 2003 Fadok 1999 Fadok and Henson 1998 Fadok et al. 1998a,b Fishelson et al. 2001 Mevorach 2003).

Ficolins Structure Function and Associated Diseases

Innate immunity relies upon the ability of a few pattern recognition molecules to sense molecular markers. Ficolins are humoral molecules of the innate immune systems which recognize carbohydrate molecules on pathogens, apoptotic and necrotic cells. Three ficolins have been identified in humans L-ficolin, H-ficolin and M-ficolin (also referred to as ficolin-2, -3 and -1, respectively). They are soluble oligomeric defence proteins with lectin-like activity and they are structurally similar to the human collectins, mannan-binding lectin (MBL) and surfactant protein A and D. Upon recognition of the infectious agent, the ficolins act through two distinct routes initiate the lectin pathway of complement activation through attached serine proteases (MASPs), and a primitive opsonophagocytosis thus limiting the infection and concurrently orchestrating the subsequent adaptive clonal immune response. Recently a lot of reports showed that dysfunction or abnormal expressions of ficolins...

Cytokine Gene Polymorphism Candidate Genes 21 Tumor Necrosis Factor

The rare allele TNF2 (A at position -308) was suggested to be linked to high TNF promoter activity (14). Autoimmune diseases like diabetes mellitus or lupus erythematosus did not show differences of allele frequencies or genotype distribution between patients and controls (20,21). In addition, patients with severe sepsis and a high proportion of Gram-negative infection also did not display altered allele frequencies concerning both biallelic promoter polymorphisms (positions -238 and -308) (22). Analysis of the TNF promoter by means of reporter gene constructs revealed contradictory results. A first report supposed a functional importance of the -308 G to A transition (14). Two articles could not confirm differences of the TNF promoter activity in relation to the -308 polymorphism (22,23). A recent article reported a possible influence on TNF promoter activity by the -308 G to A transition in a B-cell line (214). Data demonstrating an impact of this genomic polymorphism on...

Danger Transmission Through Tlrs

Immune responses that drive the production of IL-12 family cytokines. Such broad inhibition is likely to affect the host response to infection and to modulate autoimmunity. In support of this view, a central role of C5 C5a was suggested in the pathogenesis of autoimmune arthritis64, systemic lupus125, DTH responses126, and allergy123, as well as in resistance to Listeria122 and to blood stage-malaria infection128. Common to all of these models is their dependency on or exacerbation by IL-12 family cytokines. In the same report124, a suppressive effect of C5a on Th1 polarization was found the in vivo relevance of which was documented by the acquisition of resistance to Leishmania major infection by the genetic deficiency of the C5a receptor in normally susceptible BALB c mice. In this model, L. major takes advantage of the activation of one important defense mechanism of innate immunity (the complement system) to suppress cellmediated immunity induced by another crucial arm of innate...

Etiology of Fecal Incontinence

Skeletal muscle disorders such as muscular dystrophy, myasthenia gravis, and other myopathies can affect external anal sphincter and puborectalis function. Reconstructive procedures such as ileoanal or coloanal pouches can increase anorectal capacity and may improve continence 37, 38 . However, up to 40 of patients with an ileoanal pouch experience periodic, often nocturnal, fecal incontinence, possibly related to uncoordinated pouch contractions 39 . Similarly, rectal prolapse may be associated with fecal incontinence in up to 88 of cases 40-42 .

Genetic Variants Associated with CD and UC

Polymorphisms in cytokine genes and cytokine pathway genes are associated with both CD and UC. Duerr and colleagues completed the first large-scale GWAS in IBD of 308,332 SNPs 68 . A non-synonymous SNP (rs11209026 Arg381Gln) in the interleukin 23R gene conferred significant protection against IBD. Heterozygous carriage of the glutamine allele confers an approximately threefold increase in protection against developing CD, with a more modest protective effect observed in UC. Several other SNPs within IL23R were also shown to be associated with ileal CD. Further replication studies for IL23R have been published in several adult and pediatric IBD cohorts but IL23R is also associated with autoimmune diseases including psoriasis 69 and ankylosing spondylitis 70 .

Newcastle Disease Virus iParamyxoviridae

See also Apoptosis and virus infection Autoimmunity Encephalitis viruses (Fiaviviridae) Encephalitis viruses and related viruses causing hemorrhagic disease, Tick-borne encephalitis and Wesselsbron viruses Enteroviruses (Picorna-vlridae) Animal and related viruses, Human enteroviruses (serotypes 68-71) Herpes simplex viruses (Herpesvirldae) General features, Molecular biology Human immunodeficiency viruses (Retroviridae) Molecular biology, Anti-retrovirai agents, General features Human T-ceii leukemia viruses (Retroviridae) HTLV-1, HTLV-2 JC and BK viruses (Papovaviridae) Latency Lymphocytic choriomeningitis virus (Arenavirldae) General features, Molecular biology Measles virus (Para-myxoviridae) Mumps virus (Paramyxovirldae) Orbiviruses and coltiviruses (Reoviridae) General

Rescue of Autoreactive B Cells by T Cell Independent Antigens of Type I TLRLigand AntigenComplexes

In the other way, autoantigen-TLR-ligand complexes might activate immature B cells to proliferation, rather than to apoptosis of the autoantigen-specific B cells, as, for example, LPS has been seen to induce such responses on a polyclonal level with immature B cells. Thereby, autoantigen-TLR-ligand complexes could compete with autoantigen-natural IgM-complement complexes for reactions leading either to survival and proliferation or to apoptosis of the autoantigen-reactive cells. This may well occur during the peak of a bacterial infection and might become chronic if the infection is chronic. A real danger of autoimmune disease (in the case of dsDNA IgG or chromatin to SLE) should only arise if the response of the rescued, matured, activated au-toreactive B cells is taken over by a helper T cell-dependent, or otherwise AiD-inducing action of the immune system.

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