[Pathogenetic mechanisms in autoimmune diseases].
In addition to an earlier review [Z. ges. inn. Med. 35 (1980) 58] newer concepts in the pathogenesis of autoimmune diseases are presented. Acantholysis in pemphigus is caused by proteases released from cells of stratified squamous epithelium stimulated by antibodies to cell membrane antigens. The dermoepidermal cleavage in pemphigoid is presumably due to proteases from granulocytes accumulating at the dermoepidermal junction by antibody-mediated complement activation. Receptor autoantibodies can directly stimulate or block receptor function, increase cell membrane receptor degradation, or activate complement with lysis of receptor-carrying membrane structures. Tissue injury in immune complex diseases is caused by reactive oxygen metabolites and proteases released from stimulated phagocytes.
D001323:Autoantibodies / Q000032:analysis; D001327:Autoimmune Diseases / Q000276:immunology*; D001485:Basement Membrane / Q000276:immunology; D003167:Complement Activation; D003602:Cytotoxicity, Immunologic; D006023:Glycoproteins / Q000276:immunology; D006098:Granulocytes / Q000276:immunology; D006801:Humans; D007105:Immune Complex Diseases / Q000276:immunology; D010391:Pemphigoid, Bullous / Q000276:immunology; D011956:Receptors, Cell Surface / Q000276:immunology; D012871:Skin Diseases / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology
D001323:Autoantibodies; D006023:Glycoproteins; D011956:Receptors, Cell Surface
Pathogenetische Mechanismen bei Autoimmunkrankheiten.