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Description
There is increasing evidence that cellular immune abnormalities are involved in the pathogenesis of type 1 diabetes mellitus. The non-obese diabetic (NOD) mouse, a model of human type 1 diabetes, develops mononuclear cell infiltration of its pancreatic islets (insulitis), leading to /3 cell destruction and overt diabetes [l]. In recent studies, most of the islet-infiltrating cells in the NOD mouse were determined to be T cells by immunohistochemistry [2] and electron microscopy [3]. Furthermore, neonatal thymectomy [4], the administration of anti-thymocyte serum [5], or the transfer of the nude gene [6] has prevented insulitis and the development of diabetes in this animal model. These findings strongly suggest that T lymphocyte-mediated autoimmunity underlies the autoimmune phenomenon in NOD mice. Interleukin 2 (IL-2) is produced by antigenor mitogen-activated T lymphocytes and plays a central role in the development of the immune re-
Journal
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- Diabetes Research and Clinical Practice
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Diabetes Research and Clinical Practice 7 S67-S72, 1989-01-01
Elsevier BV
