[Current concepts of the predisposition and pathogenesis of exogenous allergic alveolitis].
The present conceptions about the pathogenesis of extrinsic allergic alveolitis (EAA) are summarized in a review. The development of EAA depends on both intrinsic (predisposing factors like HLA-groups etc.) and extrinsic components (nature of antigen, intensity and duration of the exposure smoking habits). Cell-mediated immunity plays a decisive role in the recognition of antigen, the induction of the pathogenic immune response (imbalance or dysregulation of T-Helper and T-Suppressor cells), in the realizing of the pathogenic effect in the lung tissue (sensitized lymphocytes, synthesis of lymphokins and interleukins with the consequent liberation of enzymes, tissue injury, granuloma-formation, fibrosis). The production of specific antibodies, the formation of immune complexes, the activation of complement system and as well as immediate irritant-toxic effects by the inhaled agents are also important in the pathogenesis of EAA.
D000542:Alveolitis, Extrinsic Allergic / Q000209:etiology* / Q000276:immunology; D000917:Antibody Formation; D000936:Antigen-Antibody Complex / Q000032:analysis; D000941:Antigens / Q000276:immunology; D004391:Dust / Q000009:adverse effects; D006680:HLA Antigens / Q000235:genetics; D006801:Humans; D007111:Immunity, Cellular; D011650:Pulmonary Alveoli / Q000276:immunology; D012907:Smoking
D000936:Antigen-Antibody Complex; D000941:Antigens; D004391:Dust; D006680:HLA Antigens
Gegenwärtige Vorstellungen zur Prädisposition und Pathogenese der exogen allergischen Alveolitis.