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病毒诱导性糖尿病的发病机制。

The pathogenesis of viral-induced diabetes.

作者信息

See D M, Tilles J G

机构信息

UC Irvine Medical Center, Department of Medicine, Orange, CA 92668, USA.

出版信息

Clin Diagn Virol. 1998 Apr;9(2-3):85-8. doi: 10.1016/s0928-0197(98)00014-2.

Abstract

Serologic case-control studies have suggested an association between coxsasckie group B viruses and insulin-dependent diabetes mellitus (IDDM). New investigations have identified enteroviral nucleic acid in the peripheral blood mononuclear cells of newly-diagnosed patients with IDDM. The disease pathogenesis is dependent on several factors. including the genetics of the host, strain of virus, activation status of autoreactive T-cells, upregulation of pancreatic MHC-1 antigens, molecular mimicry between viral and beta cell epitopes and direct islet cell destruction by viral cytolysis. Epitopes (IDDM-E1 and E2) on glutamate decarboxylase 65 (GAD65) are the most common targets for antibody and cellular-mediated autoimmune beta cell destruction.

摘要

血清学病例对照研究表明,B组柯萨奇病毒与胰岛素依赖型糖尿病(IDDM)之间存在关联。新的研究在新诊断的IDDM患者外周血单个核细胞中发现了肠道病毒核酸。该疾病的发病机制取决于多种因素,包括宿主的遗传学、病毒株、自身反应性T细胞的激活状态、胰腺MHC-1抗原的上调、病毒与β细胞表位之间的分子模拟以及病毒细胞溶解对胰岛细胞的直接破坏。谷氨酸脱羧酶65(GAD65)上的表位(IDDM-E1和E2)是抗体和细胞介导的自身免疫性β细胞破坏的最常见靶点。

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