Immune dysfunction

IMMUNE RESPONSE IN PREGNANCY

Traditionally, pregnancy from an immunological perspective, has been viewed as a conflict between the semi-allogenic fetus and the mother in which fetal survival is dependent on suppression of the maternal immune response. However, it is clear that while lymphocyte function does indeed change during pregnancy, there is no generalized suppression of the maternal immune response. Indeed, the concept of immunization of the mother, for example with paternal white blood cells, in order that she may mount a protective immune response to prevent rejection of the genetically dissimilar fetus has been refuted by randomized therapeutic studies [25].

Contemporary concepts in reproductive immunology now emphasize the co-operative nature of the interaction between individual cells and molecules of the immune system and the fetus in governing pregnancy outcome. In particular, interest is currently focused on the relationship between Natural Killer (NK) cells and reproductive failure.

Natural Killer cells are lymphocytes which are part of the innate immune system. The NK cells may be divided into those found in peripheral blood and those present in the uterine decidua. There are important phenotypic and functional differences between NK cells present at the two sites. Unlike peripheral blood NK cells, uterine NK cells have little killing ability. Micro-array analysis combined with flow cytometric and RT-PCR studies have demonstrated that the phenotype of uNK cells is different from that of NK cells in peripheral blood [26]. Hence, it may be erroneous to extrapolate data examining peripheral blood NK cells to implantation failure and RM.

While some have advocated the use of glucocoritcoids as adjuvant therapy in women with raised peripheral NK cell levels, there is no evidence base to support this.

Indeed, glucocorticoids themselves during pregnancy are associated with an increased risk of preterm delivery secondary to rupture of membranes and the development of pre-eclampsia and gestational diabetes [27]. Importantly, glucocorticoid receptors are present in the stromal compartment of the endometrium thus suggesting they play an important role in decidualization. The effect of exogenous glucocorticoid therapy on the endometrial gene expression profile during decidualization has not been examined.

The cytokine response at the maternal-fetal interface is also the subject of current investigation. This response may be broadly divided into being either a predominantly Th-1 type response (characterized by the production of inter-leukin 2, interferon-y and tumour necrosis factor-^) or a Th-2 type response (characterized by the production of interleukins -4, —6 and -10). It has been suggested that normal pregnancy is the result of a Th-2 type cytokine response which allows the production of blocking antibodies to mask fetal trophoblast antigens from immuno-logical recognition by a maternal Th-1 cell-mediated cytotoxic response [28]. In contrast, women who recurrently miscarry tend to produce a predominantly Th-1 type response both in the period of embryonic implantation and during pregnancy [29]. Immuno-modulation of the cytokine response during early pregnancy represents an important future avenue of research for therapeutic trials.

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