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首页> 外文期刊>Cell biology international. >The suppressive effect of CD25+Treg cells on Th1 differentiation requires cell-cell contact partially via TGF-beta production.
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The suppressive effect of CD25+Treg cells on Th1 differentiation requires cell-cell contact partially via TGF-beta production.

机译：CD25 + Treg细胞对Th1分化的抑制作用需要通过TGF-β产生部分地与细胞接触。

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摘要

CD25+Treg cells (CD4+CD25+Foxp3+ regulatory T cells) play a central role in the maintenance of peripheral self-tolerance and immune homoeostasis. A previous study showed that CD25+Treg cells suppressed the differentiation and function of Th1 cells in vivo and in vitro. However, the mechanism of suppressing Th1 cell differentiation mediated by CD25+Treg cells remains unclear. In the present study, we found that CD25+Treg cells could reduce the production of IFN (interferon)-gamma and the percentage of IFN-gamma-, IL-2 and TNF-alpha-producing cells by CD25-T cells under Th1 cell culture conditions and suppress the differentiation of CD25-T cells into Th1 cells in a dose-dependent manner. Moreover, these CD25+Treg cells could inhibit the activation of CD25-T cells by down-regulating the expression of activation markers CD69 and CD25 and suppress the division and proliferation of CD25-T cells using CFSE (carboxyfluorescein diacetate succinimidyl ester)-labelling and BrdU (5-bromo-20-deoxyuridine) incorporation, respectively. Further studies showed that the suppressive effects of CD25+Treg cells on Th1 cell differentiation required cell-cell contact and was partially restored by the addition of anti-TGF-beta mAb (monoclonal antibody) but not anti-IL-10 mAb, indicating that the suppression mechanism of CD25+Treg cells was cell-cell contact dependent and partially via TGF-beta. This finding strongly indicates a therapeutic role for CD25+Treg cells in Th1-mediated diseases.
机译：CD25 + Treg细胞（CD4 + CD25 + Foxp3 +调节性T细胞）在维持外周自我耐受性和免疫稳态方面起着核心作用。先前的研究表明，CD25 + Treg细胞可在体内和体外抑制Th1细胞的分化和功能。但是，抑制由CD25 + Treg细胞介导的Th1细胞分化的机制仍不清楚。在本研究中，我们发现CD25 + Treg细胞可以减少Th1细胞下CD25-T细胞产生的IFN（干扰素）-γ以及产生IFN-γ-，IL-2和TNF-α的细胞的百分比。培养条件，并以剂量​​依赖的方式抑制CD25-T细胞向Th1细胞的分化。此外，这些CD25 + Treg细胞可以通过下调激活标记CD69和CD25的表达来抑制CD25-T细胞的激活，并使用CFSE（羧基荧光素二乙酸琥珀酰亚胺酯）标记和抑制CD25-T细胞的分裂和增殖。分别引入BrdU（5-bromo-20-deoxyuridine）。进一步的研究表明，CD25 + Treg细胞对Th1细胞分化的抑制作用需要细胞间接触，并且通过添加抗TGF-βmAb（单克隆抗体）而不是抗IL-10 mAb可以部分恢复。 CD25 + Treg细胞的抑制机制是细胞间接触依赖性的，部分是通过TGF-β产生的。该发现强烈表明CD25 + Treg细胞在Th1介导的疾病中具有治疗作用。

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