Cellular immune reactions against pancreatic islets as a consequence of graft versus host disease.
We studied autoimmune reactions against pancreatic islets occurring as a consequence of defects of the immune system rather than after pathological changes in the endocrine organ itself. Immune dysregulation was induced by transfer of parental lymphocytes into semi-allogeneic F1 recipient mice (graft versus host reaction, GVHR). Recipients were killed 1 month after the induction of the disease. Pancreatic islets were screened by light microscopy for signs of lymphocytic infiltration (insulitis). Severe insulitis was found in all mice undergoing GVHR. The cytotoxic activity of lymphocytes was apparent in electron microscopic studies and affected only B cells. Infiltrations were not seen in the exocrine part of the pancreas nor in heart, liver or kidneys at this early stage of GVHR. It is concluded that non-specific disorders of the immune system induced by GVHR may lead to specific cellular autoimmune reactions against B cells of pancreatic islets.
D000818:Animals; D003602:Cytotoxicity, Immunologic; D005951:Glucose Tolerance Test; D006087:Graft vs Host Reaction; D007111:Immunity, Cellular; D007515:Islets of Langerhans / Q000276:immunology* / Q000648:ultrastructure; D017710:Lymphocyte Transfusion; D008214:Lymphocytes / Q000648:ultrastructure; D008297:Male; D051379:Mice; D008854:Microscopy, Electron; D014184:Transplantation, Homologous