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(Journal Article): Islet abnormalities in the pathogenesis of autoimmune diabetes.
Rosmalen JG, Leenen PJ, Pelegri C, Drexhage HA, Homo-Delarche F (Dept Immunology, Erasmus MC, University Medical Center, PO Box 1738, 3000 DR Rotterdam, The Netherlands.)
IN:
Trends Endocrinol Metab
2002; 13:209-214
Impact Factor(s) of Trends Endocrinol Metab: 9.058 (2004), 7.85 (2003), 5.823 (2001)
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ABSTRACT: Type 1 diabetes mellitus is a T-cell-mediated autoimmune disease that results in the destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans. In spite of extensive genetic and immunological studies, mainly performed in the non-obese diabetic (NOD) spontaneous mouse model, the etiology of the autoimmune attack remains unknown. Several autoantigens have been identified and numerous studies have suggested a role for defective regulation of immune function. However, this account does not explain why the autoimmune process specifically affects the insulin-producing beta cells. Thus, abnormal immune regulation might explain the predisposition to autoimmunity in general, but additional factors should then determine the target of the autoimmune attack. Here, we review the evidence that abnormalities in islet cell differentiation and function exist that might trigger the immune system towards beta-cell autoimmunity in humans and NOD mice.
TYPE OF PUBLICATION: Review
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