T-cell regulation in allergic reactions

Atopy is characterized by an increased tendency to form antibodies to airborne and food proteins. Specific IgE is central to the induction of allergic diseases through its binding of the high-affinity receptor on mast cells and basophils. Cross-linking by allergens of the bound IgE leads to an immediate release of various inflammatory mediators at the local site in the shock organ. Repeated exposure to allergens may lead to the induction of a more chronic inflammatory process where the local influx of T-lymphocytes and eosinophils appears to be an important event. There has been increasing recognition that cytokines, produced by a variety of inflammatory cell subsets, including T-cells, induce this ongoing inflammatory state. Besides, CD4+ T-helper-2 (Th2) cell products like IL-4 play a crucial role in the regulation of the production of specific IgE by B-cells. IL-4 appears to be the immunoregulatory cytokine with a relatively restricted action on reactive cells in this specific immune reaction. The effects of IL-4 are antagonised by IFN-gamma, and vice versa. Proliferation and differentiation of Th2 subsets producing predominantly IL-4 and IL-5 and no IFN-gamma provide an essential signal for isotype switching to IgE in B-cells, on the one hand, and direct the activation and influx of inflammatory effector cells such as eosinophils, on the other hand. In this report the causal relationship between the induction and expression of Th2 cells the IgE production and eosinophilia in atopic allergies is briefly reviewed.(ABSTRACT TRUNCATED AT 250 WORDS)