...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Adaptive TGF-β-dependent regulatory T cells control autoimmune diabetes and are a privileged target of anti-CD3 antibody treatment
【24h】

Adaptive TGF-β-dependent regulatory T cells control autoimmune diabetes and are a privileged target of anti-CD3 antibody treatment

机译：适应性TGF-β依赖性调节性T细胞可控制自身免疫性糖尿病，是抗CD3抗体治疗的优先目标

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Previous results have shown that CD4~+CD25~+ regulatory T cells (Tregs) control autoimmunity in a spontaneous model of type 1 diabetes, the nonobese diabetic (NOD) mouse. Moreover, anti-CD3 reverses diabetes in this setting by promoting Tregs that function in a TGF-β-dependent manner. This finding contrasts with a large body of work suggesting that CD4~+CD25~(high) Tregs act in a cyto-kine-independent manner, thus suggesting that another type of Treg is operational in this setting. We sought to determine the basis of suppression both in untreated NOD mice and in those treated with anti-CD3. Our present results show that a subset of foxP3~+ cells present within a CD4~+CD25~(low) lymphocyte subset suppresses T cell immunity in spontaneously diabetic NOD mice in a TGF-β-dependent manner, a functional property typical of "adaptive" regulatory T cells. This distinct Treg subset is evident in NOD, but not normal, mice, suggesting that the NOD mice may generate these adaptive Tregs in an attempt to regulate ongoing autoimmunity. Importantly, in two distinct in vivo models, these TGF-β-dependent adaptive CD4~+CD25~(low) T cells can be induced from peripheral CD4~+CD25~- T lymphocytes by anti-CD3 immunotherapy which correlates with the restoration of self-tolerance.
机译：先前的结果表明，CD4〜+ CD25〜+调节性T细胞（Tregs）在1型糖尿病自发性模型（非肥胖糖尿病（NOD）小鼠）中控制自身免疫。此外，在这种情况下，抗CD3通过促进以TGF-β依赖性方式起作用的Treg来逆转糖尿病。这一发现与大量的工作形成鲜明对比，这表明CD4〜+ CD25〜（高）Treg以细胞因子独立的方式起作用，因此表明另一种类型的Treg在这种情况下仍然有效。我们试图确定未治疗的NOD小鼠和抗CD3治疗的小鼠的抑制基础。我们目前的结果表明，存在于CD4〜+ CD25〜（低）淋巴细胞子集中的foxP3〜+细胞子集以自发性糖尿病NOD小鼠以TGF-β依赖性方式抑制T细胞免疫，这是“自适应”的典型功能特性。调节性T细胞。这种独特的Treg亚型在NOD小鼠中很明显，但在正常小鼠中却不是，这表明NOD小鼠可能会​​产生这些适应性Treg，以调节正在进行的自身免疫。重要的是，在两种不同的体内模型中，这些抗TGF-β的适应性CD4〜+ CD25〜（低）T细胞可以通过抗CD3免疫疗法从外周CD4〜+ CD25〜-T淋巴细胞中诱导，这与CD4〜+ CD25〜-T细胞的恢复有关。自我宽容。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号