Recent evidence suggests that the pathogenesis of insulindependent (type I, juvenile onset) diabetes mellitus may have an important autoimmune component, possibly triggered by a viral infection. This evidence includes mononuclear infiltration of the endocrine pancreas, circulating islet cell antibodies, and a strong association with certain HLA alleles (DR3 and DR4). The biologic response (apart from allograft rejection) of diabetic hosts to transplanted islets has been examined in an animal model of spontaneous diabetes which closely resembles the human condition (the BB rat). In this syndrome, MHC‐compatible islet allografts suffered autoimmune destruction even when rejection was excluded by experimental design. Implications of this finding with respect to human islet and/or pancreas transplantation are discussed.
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Naji et al. (1984) studied this question.
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