The anti-IgE/anti-Fc epsilon RI alpha autoantibody network in allergic andautoimmune diseases

Basophil granulocytes and tissue mast cells and their mediators play a role in the pathogenesis of several immune and inflammatory disorders. Human ba sophils and mast cells (Fc epsilon RI+ cells) can be activated through immu nological interaction with the IgE-Fc epsilon RI network. Fc epsilon RI+ ce lls can be triggered by cross-linking between the Fab portions of IgE and m ultivalent antigens (direct anaphylaxis). 'Reverse type' anaphylaxis can oc cur through three distinct mechanisms: antibodies against the Fc epsilon po rtion of IgE (anti-IgE), antibodies against epitopes of the or chain of Fc epsilon RI (anti-Fc epsilon RI alpha) and anti-IgG acting on IgG-IgE comple xes bound to Fc epsilon RI. Anti-IgE autoantibodies are occasionally presen t even in normal donors and more frequently in a variety of allergic (chron ic urticaria, atopic dermatitis and bronchial asthma) and autoimmune disord ers (rheumatoid arthritis, lupus erythematosus and systemic sclerosis). IgG anti-IgE from a small percentage of patients induces the release of mediat ors from human Fc epsilon RI+ cells. Some of the anti-IgE autoantibodies pr esent in allergic patients are non-anaphylactogenic, thus representing a po ssible protective mechanism preventing the association of IgE with Fc epsil on RI. Anti-Fc epsilon RI alpha autoantibodies also occur in a significant percentage of patients of chronic urticaria and probably non-allergic asthm a and some autoimmune diseases. Although anti-IgE and anti-Fc epsilon RI al pha autoantibodies, present in a percentage of patients with immune disorde rs, are relevant to the pathogenesis of these conditions, much remains to b e learnt about their immunochemistry, their prevalence and precise role in various inflammatory diseases.