Cutting edge:: TGF-β signaling is required for the in vivo expansion and immunosuppressive capacity of regulatory CD4+ CD25+ T cells
Cutting edge:: TGF-β signaling is required for the in vivo expansion and immunosuppressive capacity of regulatory CD4+ CD25+ T cells
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DOI：
10.4049/jimmunol.173.11.6526
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发表时间：
2004-12-01
影响因子：
4.4
通讯作者：
Blessing, M
中科院分区：
文献类型：
--
作者：
Huber, S;Schramm, C;Blessing, M
关于 TGF-β 对调节性 CD4(+)CD25(+) T 细胞 (Treg) 体内功能的作用的数据存在争议。在硫酸葡聚糖诱导的结肠炎小鼠模型中，使用T细胞中TGF-β信号传导受损的转基因小鼠模型来评估内源性TGF-β对CD4(+)CD25(+)Treg体内功能的作用。研究发现，野生型而非转基因 CD4(+) CD25(+) Treg 的转移可抑制野生型小鼠的结肠炎。此外，通过转移ME标记的CD4(+)CD25(+) Treg，我们可以证明内源性TGF-β促进CD4(+)CD25(+) Treg在体内的扩增。转基因小鼠本身外周CD4(+)CD25(+) Treg数量减少，并且更容易诱发结肠炎，这可以通过转移野生型Treg来预防。这些数据表明，CD4(+)CD25(+) Treg 中的 TGF-β 信号传导是其体内扩张和抑制能力所必需的。
Data regarding the role of TGF-beta for the in vivo function of regulatory CD4(+)CD25(+) T cells (Treg) are controversial. A transgenic mouse model with impaired TGF-beta signaling specifically in T cells was used to assess the role of endogenous TGF-beta for the in vivo function of CD4(+) CD25(+) Treg in a murine model of colitis induced by dextran sulfate. Transfer of wild-type, but not transgenic CD4(+) CD25(+) Treg was found to suppress colitis in wild-type mice. In addition, by transferring ME-labeled CD4(+)CD25(+) Treg we could demonstrate that endogenous TGF-beta promotes the expansion of CD4(+)CD25(+) Treg in vivo. Transgenic mice themselves developed reduced numbers of peripheral CD4(+)CD25(+) Treg and were more susceptible to the induction of colitis, which could be prevented by the transfer of wild-type Treg. These data indicate that TGF-beta signaling in CD4(+)CD25(+) Treg is required for their in vivo expansion and suppressive capacity.