Non-obese-diabetic mice: immune mechanisms of pancreatic beta-cell destruction.
The sequence of events shortly before the initiation of diabetes in female non-obese diabetic mice was studied. Immunologically, anti-lymphocyte antibodies appeared most frequently at 3 weeks of age and decreased thereafter. Insulin concentrations dropped after the initiation of mononuclear cell infiltration into the islets. The majority of female mice lost approximately 85% of their insulin at aged 22 weeks. Islet cell surface antibodies appeared most frequently during this period (12-18 weeks). Morphological examination revealed that mononuclear cells start to infiltrate islets at 6 weeks of age and involve major areas of the islets in females aged 22 weeks. Among these mononuclear cells, IgM-positive cells were found to be a major constituent, forming follicular (nodular) cell aggregates. T-helper and/or T-cytotoxic cells (Lyt-1-, and/or Lyt-2-positive cells) were fewer and located mainly around the follicular structures. Asialo GM 1-positive lymphocytes (natural killer cells), though present, were far fewer. The process of destruction of pancreatic islets in non-obese diabetic mice is discussed with emphasis on the characteristic local immune response in the pancreas.
D000818:Animals; D000917:Antibody Formation; D001323:Autoantibodies / Q000096:biosynthesis; D003602:Cytotoxicity, Immunologic; D003921:Diabetes Mellitus, Experimental / Q000276:immunology*; D005260:Female; D007515:Islets of Langerhans / Q000276:immunology* / Q000473:pathology; D008214:Lymphocytes / Q000276:immunology; D008297:Male; D051379:Mice; D013997:Time Factors
D001323:Autoantibodies; C024211:islet cell antibody