Mechanisms of rat pancreatic islet allograft rejection.
Since the mechanisms of rat islet allograft rejection are unknown, metabolic, histologic, and immunologic parameters were characterized during rejection. Syngeneic intraportal islet transplants in diabetic Lewis rats normalize glucose values without islet cellular infiltrates; after Wistar-Furth allografts, glucose values rapidly return to diabetic levels and infiltration of islets by mononuclear cells occurs. Using lymphocyte proliferative assays, allogeneic islets induce a 3-fold stimulation of lymphocytes derived from nondiabetic allograft recipients. Using cytotoxicity assays, cell-mediated cytotoxicity of allogeneic islet target cells although inefficient is 2-fold greater in diabetic allograft recipients than in syngeneic recipients. Antibody-dependent cellular cytotoxicity is not observed, whereas 14 days after allotransplantation, complement-dependent antibody-mediated cytotoxicity is elevated. These data suggest that islet allograft rejection using metabolic, histopathologic and immunologic methods is associated primarily with cell-mediated cytotoxicity related to histocompatibility antigens.
D000818:Animals; D000920:Antibody-Dependent Cell Cytotoxicity; D003921:Diabetes Mellitus, Experimental / Q000276:immunology*; D006084:Graft Rejection; D006649:Histocompatibility Antigens / Q000276:immunology; D007111:Immunity, Cellular; D016381:Islets of Langerhans Transplantation; D008213:Lymphocyte Activation; D008297:Male; D051381:Rats; D011917:Rats, Inbred Lew; D011920:Rats, Inbred WF; D013311:Streptozocin
D006649:Histocompatibility Antigens; D013311:Streptozocin