Non-obese-diabetic mice: immune mechanisms of pancreatic β-cell destruction

Y Kanazawa, K Komeda, S Sato, S Mori, K Akanuma… - Diabetologia, 1984 - Springer
Y Kanazawa, K Komeda, S Sato, S Mori, K Akanuma, F Takaku
Diabetologia, 1984Springer
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 …
Summary
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 GM1-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.
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