Failure of a protective major histocompatibility complex class II molecule to delete autoreactive T cells in autoimmune diabetes.
Failure of a protective major histocompatibility complex class II molecule to delete autoreactive T cells in autoimmune diabetes.
复制标题
保护性主要组织相容性复合物 II 类分子未能删除自身免疫性糖尿病中的自身反应性 T 细胞。
DOI：
10.1073/pnas.90.22.10808
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发表时间：
1993
影响因子：
11.1
通讯作者：
Brett Charlton
中科院分区：
文献类型：
--
作者：
Robyn M. Slattery;Jacques F. A. P. Miller;William R. Heath;Brett Charlton
The association of major histocompatibility complex genes with autoimmune diseases is firmly established, but the mechanisms by which these genes confer resistance or susceptibility remain controversial. The controversy extends to the nonobese diabetic (NOD) mouse that develops disease similar to human insulin-dependent diabetes mellitus. The transgenic incorporation of certain class II major histocompatibility complex genes protects NOD mice from diabetes, and clonal deletion or functional silencing of autoreactive T cells has been proposed as the mechanism by which these molecules provide protection. We show that neither thymic deletion nor anergy of autoreactive T cells occurs in NOD mice transgenic for I-Ak. Autoreactive T cells are present, functional, and can transfer diabetes to appropriate NOD-recipient mice.
