Insulin-Dependent Diabetes Mellitus as an Autoimmune Disease

作者: JEAN-FRANÇOIS BACH

DOI: 10.1210/EDRV-15-4-516

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摘要: IDDM is unquestionably an autoimmune disease, as reflected by the presence of beta-cell-reactive autoantibodies and T cells, cell-mediated transfer disease in nondiabetic mice, rats, humans, sensitivity to immunosuppressive therapy. cells are predominantly, if not exclusively, involved creating islet lesions that lead beta-cell atrophy after a stage reversible inflammation. A full understanding pathogenesis will require better definition nature triggering target autoantigen(s) effector mechanisms (cytokines, cytotoxic cells?). Much less information available on etiology than pathogenesis. Genetic factors mandatory involvement predisposition genes (HLA non-HLA) now being unravelled. The modulatory role environmental demonstrated high discordance rate identical twins experimental data showing positive negative modulation number agents, notably infectious agents food constituents. It clear, however, whether given factor, e.g. precise virus or cow's milk component, plays real etiological selected genetic background. thus appears multifactorial disease. known, all intervene concomitantly individual separately subsets patients, explaining clinical heterogeneity underlying loss tolerance self still unknown. Defective intrathymic selection autoantigen-specific autoreactive cell clones unlikely. Breakdown anergy could occur according various mechanisms, including aberrant expression MHC molecules molecular mimicry. suppressor function, perhaps related TH1/TH2 imbalance, probably intervenes amplifying anti-beta-cell response whatever its mechanism. Before putative identified, one must base immunotherapy nonantigen-specific agents. Results recently obtained NOD mice indicate goal nontoxic long-lasting immune protection from feasible treatment started early enough. In some cases (anti-T monoclonal antibodies), it specific unresponsiveness can be induced. This double strategy (early intervention, induction) main challenge for immunodiabetologists.(ABSTRACT TRUNCATED AT 400 WORDS)

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