Immunological mechanisms

Type I: IgE-mediated reactions

These reactions are the most frequent, the best known and the easiest to diagnose. They occur when an individual is already sensitised. In susceptible individuals, when a food allergen is encountered for the first time, the adaptive response initiates production of IgE antibodies. IgE antibody production itself is regulated and depends upon compounds known as cytokines.

Once IgE antibodies are produced, they will bind to mast cells. This process, known as sensitisation, precedes symptoms of allergy. How early in life an individual can be sensitised has been a topic of much interest lately. Some would argue that sensitisation can take place in utero. The second stage following sensitisation can take place weeks or sometimes years later. This stage occurs when the individual encounters the same food allergen for the second time. The allergen will encounter the mast cells, which already possess allergen-specific antibodies on their surface. IgE antibodies will bind the allergen and this will lead to mast-cell degranulations and release of mediators such as histamine, and the characteristic features of allergic disease follow.8 These include:

urticaria (this is the specific term used for hives, which are red, itchy skin welts brought on by an allergic reaction)

angioedema (this condition often co-exists with urticaria and usually happens when urticaria affects deeper tissues and swelling results; the most common sites are lips, tongue, eyelids and larynx)

• hypotension (low blood pressure)

• anaphylaxis (this is a severe reaction with a rapid onset causing circulatory collapse, hypotension and suffocation due to tracheal swelling).

Type II: Non-IgE-mediated reactions

Here the adverse reaction is the consequence of an immune response other than IgE. It could involve another class of immunoglobulins, or food immune complexes, or cell-mediated immunity. Other immunoglobulins implicated are IgG and their subclasses. IgG4 to specific foods are often detected in those with adverse reactions to food.9,10 The problem is that these antibodies are quite common, in both healthy and diseased states, and are often detected in normal subjects.11 Their presence in both allergic and non-allergic individuals is explained by the immune system's ability to produce IgG.12 Knowing the amount of food we eat, it is not surprising that IgG4 antibodies have been demonstrated. Some suggest that the presence of IgG4 alone reflects dietary intake, and the presence of both IgG4 and IgE reflects sensitisation in the individual.13 Further studies are needed to establish the contribution of IgG4 towards immune reactions to foods.

Type III: Immune complex-mediated reactions

These reactions are also referred to as Type III hypersensitivity reactions. When we eat, food proteins that are absorbed encounter specific antibodies in the circulation and form complexes.14,15 These are known as immune complexes. It appears that immune complex formation is essentially a normal process that occurs in the course of an immune response and allows antigen clearing. These food immune complexes contain IgE, IgG and IgA antibodies. They are usually cleared very quickly by our reticulo-endothelial system. The pathology is caused when these complexes are deposited in certain tissue sites. Their pathogenic potential is determined partly by their size and partly by their concentrations. If these food antigens and immune complexes are present in very high concentrations, tissue damage can occur. This damage is done by activation of complement, releasing C5a to create a local inflammatory response and hence increasing vascular permeability, which allows fluids and cells to enter the site. Although circulating immune complexes containing food antigen have been demonstrated in patients with food allergy suffering from asthma and eczema, there is no definitive evidence that either IgG or IgE food immune complexes cause the disease.16

Type IV: Cell-mediated food allergy

These reactions are sometimes referred to as Type IV or delayed-type hypersensitivity reactions. They are mediated by inflammatory T cells. There are reports of cell-mediated immune responses to food antigens in cow's milk allergy. There is also good evidence to suggest that coeliac disease may be provoked by a cell-mediated food allergy to gliadin, a constituent part of gluten.17 The characteristic hyperplastic villous atrophy in coeliac disease is secondary to an abnormal T cell-mediated response to gliadin. Although T cells have been shown to be involved in coeliac disease,18 there is little evidence to suggest that cell-mediated food allergy to gliadin is the original cause of coeliac disease.

It is important to consider that these immune mechanisms are not mutually exclusive and more than one mechanism may very well operate at any one time.

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