期刊
CURRENT OPINION IN IMMUNOLOGY
卷 20, 期 1, 页码 111-118出版社
CURRENT BIOLOGY LTD
DOI: 10.1016/j.coi.2007.11.005
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- NIAID NIH HHS [U19 AI050864, U19 AI050864-07, AI50864] Funding Source: Medline
- NIDDK NIH HHS [DK064605, R01 DK032083-25, DK62718, DK32493, P30 DK57516, R01 DK032493, K08 DK064605, R01 DK055969-09, DK32083, R01 DK055969, DK55969, R37 DK032083, R37 DK032493, R01 DK032083, R01 DK062718, P30 DK057516] Funding Source: Medline
Although multiple islet autoantigens are recognized by T lymphocytes and autoantibodies before the development of type 1A (immune-mediated diabetes), there is increasing evidence that autoimmunity to insulin may be central to disease pathogenesis. Evidence is strongest for the NOD mouse model where blocking immune responses to insulin prevents diabetes, and insulin peptides can be utilized to induce diabetes. In man insulin gene polymorphisms are associated with disease risk, and autoantibodies and T cells reacting with multiple insulin/proinsulin epitopes are present. It is not currently clear why insulin autoimmunity is so prominent and frequent, and though insulin can be used to immunologically prevent diabetes of NOD mice, insulin-based preventive immunoregulation of diabetes in man is not yet possible.
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