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胰岛素依赖型糖尿病:胰岛细胞抗原与微生物之间的分子模拟假说。

Insulin-dependent diabetes mellitus: the hypothesis of molecular mimicry between islet cell antigens and microorganisms.

作者信息

Maclaren N K, Alkinson M A

机构信息

New Orleans Research Institute, New Orleans Children's Hospital, LA 70118, USA.

出版信息

Mol Med Today. 1997 Feb;3(2):76-83. doi: 10.1016/s1357-4310(96)10056-3.

Abstract

Insulin-dependent diabetes mellitus (IDDM) in humans and the non-obese diabetic mouse is a polygenic disease, resulting from an autoimmune destruction of the insulin-secreting pancreatic beta cells. At least in NOD mice, the process is mediated through a T helper 1-cell-mediated cytotoxicity pathway. Although there is much circumstantial evidence to suggest that IDDM is environmentally induced, recent studies support the possibility that the inductive event involves cross-reactive immune responses to antigenic epitopes acting as molecular mimics between microbial proteins and autoantigens expressed by pancreatic insulin-secreting beta cells. The following article reviews the evidence for this concept.

摘要

人类的胰岛素依赖型糖尿病(IDDM)以及非肥胖型糖尿病小鼠所患的糖尿病是一种多基因疾病,由分泌胰岛素的胰腺β细胞的自身免疫性破坏所致。至少在非肥胖型糖尿病(NOD)小鼠中,该过程是通过辅助性T1细胞介导的细胞毒性途径介导的。尽管有许多间接证据表明IDDM是由环境因素诱发的,但最近的研究支持这样一种可能性,即诱发事件涉及对充当微生物蛋白和胰腺胰岛素分泌β细胞表达的自身抗原之间分子模拟物的抗原表位的交叉反应性免疫应答。以下文章综述了这一概念的证据。

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