The pathogenesis of IgE mediated allergies has been elucidated. We are dealing primarily with diseases of the T lymphocyte system. Due to overactivity of so-called T helper lymphocytes there is pathologic overproduction of IgE and inflammatory cells, mast cells and eosinophils, after antigen contact. Following exposure to nutrient and inhalant allergens in the presence of adjuvants, this atopic constitution manifests itself clinically. Mast cell mediators (e.g. histamine and leukotrienes) elicit immediate symptoms at the ports of entrance of allergens (at skin and mucosal surfaces); eosinophil mediators (e.g. platelet activating factor [PAF], eosinophil cationic protein [ECP], and major basic protein [MBP]) are responsible for late symptoms and hyperreactivity. Current antiinflammatory treatment tries to suppress this allergic inflammation (e.g. with cromoglycate and topical steroids). The regulatory immunotherapy of the near future attempts to regulate IgE synthesis by interleukins (e.g. gamma-Interferon) or antagonists of interleukins (e.g. anti-IL-4-antibodies).