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首页> 外文期刊>Nature immunology >Absence of signaling into CD4 + cells via C3aR and C5aR enables autoinductive TGF-β1 signaling and induction of Foxp3 + regulatory T cells
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Absence of signaling into CD4 + cells via C3aR and C5aR enables autoinductive TGF-β1 signaling and induction of Foxp3 + regulatory T cells

机译：通过C3aR和C5aR进入CD4 +细胞的信号转导的缺失可以实现自诱导TGF-β1信号转导和Foxp3 +调节性T细胞的诱导

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摘要

Signaling through the G protein-coupled receptors for the complement fragments C3a and C5a (C3aR and C5aR, respectively) by dendritic cells and CD4 + cells provides costimulatory and survival signals to effector T cells. Here we found that when signals from C3aR and C5aR were not transduced into CD4 + cells, signaling via the kinases PI(3)Kγ, Akt and mTOR ceased, activation of the kinase PKA increased, autoinductive signaling by transforming growth factor-β1 (TGF-β1) initiated and CD4 + T cells became Foxp3 + induced regulatory T cells (iT reg cells). Endogenous TGF-β1 suppressed signaling through C3aR and C5aR by preventing the production of C3a and C5a and upregulating C5L2, an alternative receptor for C5a. The absence of signaling via C3aR and C5aR resulted in lower expression of costimulatory molecules and interleukin 6 (IL-6) and more production of IL-10. The resulting iT reg cells exerted robust suppression, had enhanced stability and suppressed ongoing autoimmune disease. Antagonism of C3aR and C5aR can also induce functional human iT reg cells.
机译：树突状细胞和CD4 +细胞通过补体片段C3a和C5a（分别为C3aR和C5aR）的G蛋白偶联受体发出信号，为效应T细胞提供了共刺激信号和存活信号。在这里我们发现，当来自C3aR和C5aR的信号未转导至CD4 +细胞时，通过激酶PI（3）Kγ，Akt和mTOR的信号传导停止了，激酶PKA的激活增加了，通过转化生长因子β1（TGF -β1）启动，CD4 + T细胞变成Foxp3 +诱导的调节性T细胞（iT reg细胞）。内源性TGF-β1通过阻止C3a和C5a的产生并上调C5L2（C5a的另一种受体）而抑制了通过C3aR和C5aR的信号传导。通过C3aR和C5aR缺乏信号传导会导致共刺激分子和白介素6（IL-6）的表达降低，并产生更多的IL-10。所得的iT reg细胞具有强大的抑制作用，具有增强的稳定性并抑制了正在进行的自身免疫性疾病。 C3aR和C5aR的拮抗作用也可以诱导功能性人iT reg细胞。

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