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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Unique role of CD4~+CD62L~+ regulatory T cells in the control of autoimmune diabetes in T cell receptor transgenic mice
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Unique role of CD4~+CD62L~+ regulatory T cells in the control of autoimmune diabetes in T cell receptor transgenic mice

机译：CD4〜+ CD62L〜+调节性T细胞在控制T细胞受体转基因小鼠自身免疫性糖尿病中的独特作用

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Converging experimental evidence indicates that CD4~+ regulatory T cells control progression of autoimmune insulitis in nonobese diabetic (NOD) mice. Here, we studied the nature of these regulatory T cells and their mode of action in diabetes-prone NOD Rag~(-/-)or severe combined immunodef icient (SCID) mice harboring a transgenic T cell receptor derived from the diabetogenic T cell clone BDC2.5. We first show that diabetes onset is prevented in such mice by infusion of polyclonal CD4~+ T cells expressing L-selectin (CD62L) but not prevented or only marginally prevented by CD4~+CD25~+ T cells. Similarly, we found with a cotransfer model that CD4~+CD62L~+ T cells but not CD4~+CD25~+ T cells inhibited diabetes transfer into NOD SCID recipients by transgenic NOD BDC2.S SCID cells. Unexpectedly, cotransfer of transgenic NOD BDC2.5 SCID cells and spleen cells from WT diabetic NOD mice did not induce diabetes, whereas each individual population did so. Data are presented arguing for the role of CD4~+CD62L~+ T cells present within the polyclonal diabetogenic population in mediating this apparently paradoxical effect. Collectively, these data confirm the central role of CD4~+CD62L~+ regulatory T cells in controlling disease onset in a well defined transgenic model of autoimmune diabetes and suggest the intervention of homeostatic mechanisms as part of their mode of action.
机译：越来越多的实验证据表明，CD4 +调节性T细胞可控制非肥胖糖尿病（NOD）小鼠自身免疫性胰岛素炎的进展。在这里，我们研究了这些调节性T细胞的性质及其在易发糖尿病的NOD Rag〜（-/-）或携带源自糖尿病性T细胞克隆的转基因T细胞受体的严重联合免疫缺陷（SCID）小鼠中的作用方式BDC2.5。我们首先显示，通过输注表达L-选择素（CD62L）的多克隆CD4〜+ T细胞可预防这类小鼠的糖尿病发作，但CD4〜+ CD25〜+ T细胞不能预防或仅能预防。同样，我们通过共转移模型发现，CD4〜+ CD62L〜+ T细胞而非CD4〜+ CD25〜+ T细胞通过转基因NOD BDC2.S SCID细胞抑制了糖尿病向NOD SCID受体的转移。出乎意料的是，来自野生型糖尿病NOD小鼠的转基因NOD BDC2.5 SCID细胞和脾细胞的共转移没有诱导糖尿病，而每个个体都诱导了糖尿病。提出的数据表明存在于多克隆糖尿病形成人群中的CD4〜+ CD62L〜+ T细胞在介导这种明显矛盾的作用中的作用。总的来说，这些数据证实了CD4 + CD62L +调节性T细胞在良好定义的自身免疫性糖尿病转基因模型中在控制疾病发作中的核心作用，并暗示了稳态机制的干预作为其作用方式的一部分。

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