Inflammatory Destruction of Pancreatic β Cells in γ-Interferon Transgenic Mice

  1. N. Sarvetnick*,
  2. J. Shizuru,
  3. D. Liggitt*, and
  4. T. Stewart*
  1. *Department of Developmental Biology, Genentech, Inc., South San Francisco, California 94080; Department of Medicine, Division of Immunology and Rheumatology, Stanford University Medical Center, Stanford, California 94305

This extract was created in the absence of an abstract.

Excerpt

The lesion “insulitis” was originally described by Gepts (1965) as a discrete accumulation of lymphocytes within and surrounding the islets of newly diagnosed, insulin-dependent diabetic patients. This was perhaps the first indication that human diabetes can be mediated by the cellular immune system, resulting in the loss of insulin-producing β cells from pancreatic islets. A similar inflammatory lesion has also been observed in nonobese diabetic (NOD) mice (Like and Weringer 1988) and BB rats (Tarui et al. 1986), two animal models of insulin-dependent diabetes mellitus (IDDM). The presence of antibodies directed against islet cell components has also been demonstrated in both humans and animal models (Sai et al. 1984), and these antibody data suggest that the immune sensitization to specific islet cellular components might be involved in the onset of the disease. Additionally, there is a strong genetic correlation with susceptibility to the disease (Arnheim et al. 1985; Sheehy et...

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