1型糖尿病:慢性进行性自身免疫性疾病。

Li Zhang, Roberto Gianani, Maki Nakayama, Edwin Liu, Masakazu Kobayashi, Erin Baschal, Liping Yu, Sunanda Babu, Abby Dawson, Kelly Johnson, Mohamed Jahromi, Theresa Aly, Pamela Fain, Jennifer Barker, Marian Rewers, George S Eisenbarth
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引用次数: 32

摘要

动物模型的大量数据表明,1A型糖尿病是由T细胞介导的胰岛β细胞特异性破坏引起的。NOD小鼠模型的证据表明,胰岛素是主要的自身抗原,特异性胰岛素肽B:9-23是发病的核心。现在也可以通过遗传、免疫和代谢参数的组合来预测绝大多数个体的1A型(免疫介导的)糖尿病的发展。这种预测是可能的,因为自身免疫的慢性性质和疾病之前β细胞功能的丧失。鉴于能够预测1A型糖尿病的所有阶段的试验,以防止细胞破坏现在是可能的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Type 1 diabetes: chronic progressive autoimmune disease.

A wealth of data in animal models indicates that type 1A diabetes results from T cell-mediated specific destruction of islet beta cells. There is evidence for the NOD mouse model that insulin is the primary autoantigen and a specific insulin peptide B:9-23 is central to pathogenesis. It is also now possible to predict the development of type 1A (immune mediated) diabetes for the great majority of individuals with a combination of genetic, immunological and metabolic parameters. Such prediction is possible because of the chronic nature of the autoimmunity and loss of beta cell function that precedes the disease. Given the ability to predict type 1A diabetes trials at all stages of the disorder to prevent beta cell destruction are now possible.

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