Immunological events in new onset diabetes.
Data from our laboratory are reviewed showing that both cell-mediated cytotoxicity, complement-dependent antibody-mediated cytotoxicity, antibody-dependent cellular cytotoxicity, and complement-augmented antibody-dependent cellular cytotoxicity may provide mechanisms which kill pancreatic islets during pathogenesis of insulin-dependent (type I) diabetes. Xenogenic test systems employing dispersed rat islet target cells were employed. Most of the findings were reversible during clinical remission of diabetes.
D000818:Animals; D000920:Antibody-Dependent Cell Cytotoxicity; D003167:Complement Activation; D003165:Complement System Proteins / Q000276:immunology; D003602:Cytotoxicity, Immunologic; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D006801:Humans; D066298:In Vitro Techniques; D007515:Islets of Langerhans / Q000276:immunology*; D007962:Leukocytes / Q000276:immunology; D011817:Rabbits; D051381:Rats
D003165:Complement System Proteins