Pathophysiologicl aspects of immune complex diseases part i. interaction with plasma enzyme systems, cell membranes and the immune response.
Immune complexes (IC) may be pathophysiologically active in correlation with the nature and size of the antigen, the type and the quality of the antibody, and the concentration of both. Those parameters are decisive for the composition and the lattice structure of IC. Pathogenic effects are induced: by complement activation and generation of biologically active C' split products via the classical and the alternative pathway, by interaction with Fc and complement receptors resulting in exocytosis of lysosomal contents including degradative enzymes, cationic proteins, vasoactive amines and mediators effective on lymphocytes and macrophages; by direct and indirect activation of the Hageman factor followed by stimulation of the kinin, coagulation and fibrinolysis system; and by modulation of the immune response via the afferent and the efferent branch. All those mechanisms seen to be involved in the induction of lesions along the vessel wall in the various privileged organs.
D000917:Antibody Formation; D000936:Antigen-Antibody Complex; D001667:Binding, Competitive; D002462:Cell Membrane / Q000187:drug effects; D003167:Complement Activation; D004789:Enzyme Activation; D005174:Factor XII; D006098:Granulocytes / Q000187:drug effects; D006801:Humans; D007165:Immunosuppression Therapy; D008264:Macrophages / Q000187:drug effects; D011951:Receptors, Complement; D011961:Receptors, Fc
D000936:Antigen-Antibody Complex; D011951:Receptors, Complement; D011961:Receptors, Fc; D005174:Factor XII