Damage control, rather than unresponsiveness, effected by protective DX5+T cells in autoimmune diabetes
Damage control, rather than unresponsiveness, effected by protective DX5+T cells in autoimmune diabetes
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DOI：
10.1038/ni738
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发表时间：
2001-12-01
影响因子：
30.5
通讯作者：
Benoist, C
中科院分区：
文献类型：
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作者：
Gonzalez, A;Andre-Schmutz, I;Benoist, C
自身免疫性糖尿病的进展受到调节。我们在这里检查了对 BDC2.5 T 细胞受体转基因模型中发生的疾病施加的细胞控制。我们发现，所有具有单克隆、β 细胞反应性 T 细胞库的 BDC2.5 小鼠在 4 周龄前均患上糖尿病；将年轻标准 NOD（非肥胖糖尿病）小鼠的脾细胞转移到围产期单克隆 BDC2.5 动物中可以保护它们免受糖尿病的影响。保护活性由 CD4(+) αβ T 细胞产生，该细胞在疾病发生时工作时间很短，可以根据 DX5 细胞表面标志物的表达进行分配并分为两个部分。保护不涉及自身反应性 BDC2.5 细胞的克隆删除或无反应性，从而允许它们完全激活并攻击胰岛；相反，它减轻了胰岛素样病变的侵袭性和β细胞破坏的程度。
The progression of autoimmune diabetes is regulated. We examined here the cellular controls exerted on disease that developed in the BDC2.5 T cell receptor-transgenic model. We found that all BDC2.5 mice with a monoclonal, beta cell-reactive,T cell repertoire developed diabetes before 4 weeks of age; transfer of splenocytes from young standard NOD (nonobese diabetic) mice into perinatal monoclonal BDC2.5 animals protected them from diabetes. The protective activity was generated by CD4(+) alpha beta T cells, which operated for a short time at disease initiation, could be partitioned according to DX5 cell surface marker expression and split into two components. Protection did not involve clonal deletion or anergy of the autoreactive BDC2.5 cells, permitting their full activation and attack of pancreatic islets; rather, it tempered the aggressiveness of the insulitic lesion and the extent of beta cell destruction.