Beta cell MHC class I is a late requirement for diabetes
Beta cell MHC class I is a late requirement for diabetes
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DOI：
10.1073/pnas.1131954100
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发表时间：
2003-05-27
影响因子：
11.1
通讯作者：
Slattery, RM
中科院分区：
文献类型：
--
作者：
Hamilton-Williams, EE;Palmer, SE;Slattery, RM
1 型糖尿病是由于自身免疫攻击产生胰岛素的 β 细胞而发生的。尽管 CD8 T 细胞在这一过程的早期和晚期都有涉及，但这些细胞与 β 细胞上的 MHC I 类直接相互作用的必要性尚未得到证实。通过使用缺乏 I 类 β 细胞表达的非肥胖糖尿病小鼠，我们发现胰岛素炎的发生和进展均不受干扰。然而，如果没有 I 类 β 细胞表达，这些小鼠中的绝大多数不会出现高血糖。这些发现表明，CD8 T 细胞和 β 细胞之间的直接相互作用并不是疾病发生或早期进展所必需的。对 β 细胞的 I 类需求是糖尿病发展过程中相对较晚的检查点。
Type 1 diabetes occurs as a result of an autoimmune attack on the insulin-producing beta cells. Although CD8 T cells have been implicated both early and late in this process, the requirement for direct interaction between these cells and MHC class I on the beta cells has not been demonstrated. By using nonobese diabetic mice lacking beta cell class I expression, we show that both initiation and progression of insulitis proceeds unperturbed. However, without beta cell class I expression, the vast majority of these mice do not develop hyperglycemia. These findings demonstrate that a direct interaction between CD8 T cells and beta cells is not required for initiation or early disease progression. The requirement for class I on beta cells is a relatively late checkpoint in the development of diabetes.