[Immune response and pathophysiology of the allergic reaction]

The allergic immune response is characterized by a number of cellular and molecular interactions. Allergens are taken up through the respiratory or digestion tract or the skin by dendritic cells, B cells or macrophages. After phagocytoses and processing, fragments of allergens are presented to the allergen-specific T cells. By this process, allergen-reactive T cells are induced, which are predominantly of the Th2 type and which secrete the cytokines IL-4, IL-5 and IL-10. In contrast, during a normal immune response to bacterial or viral allergens, T cells of the Th1 type are induced, which produce IFN gamma and IL-2 but not Th2 cytokines. A direct contact of Th2 cells with B cells results in activation of B cells. The Th2 cytokine IL-4 instructs B cells to switch from IgM to IgE antibody production. IgE antibodies play a central role in the induction of allergic diseases. IgE antibodies are taken up by basophils and mast cells by virtue of high-affinity receptors for IgE on these cells. Allergen confrontation leads to the activation of such IgE-sensitized cells, which results in the release of various mediators such as histamine, leukotrienes and prostaglandins; together, they induce the clinical manifestations of allergic reactions. Recent findings have shown that mast cells (and basophils) from atopic tissue are able to produce cytokines such as IL-4 and can thereby induce IgE antibody production. IL-5 generated by allergen-reactive Th2 cells attracts and activates eosinophils, which are responsible for tissue destruction in allergic asthma.(ABSTRACT TRUNCATED AT 250 WORDS)