The regulation of regulation: interleukin-10 increases CD4+ CD25+ regulatory T cells but impairs their immunosuppressive activity in murine models with schistosomiasis japonica or asthma
The regulation of regulation: interleukin-10 increases CD4+ CD25+ regulatory T cells but impairs their immunosuppressive activity in murine models with schistosomiasis japonica or asthma
复制标题
调节的调节：在日本血吸虫病或哮喘小鼠模型中，白介素 10 会增加 CD4( ) CD25( ) 调节性 T 细胞，但会损害其免疫抑制活性。
DOI：
10.1111/imm.12813
复制
发表时间：
2018-01-01
期刊：
影响因子：
6.4
通讯作者：
Su, Chuan
中科院分区：
文献类型：
--
作者：
He, Lei;Zhou, Sha;Su, Chuan
CD4(+)CD25(+)Foxp3(+)调节性T细胞(Treg)在维持免疫平衡中起着重要作用。白介素10(IL-10)是一种具有抗炎功能的细胞因子，在控制免疫反应中也起着关键作用。此外，众所周知，IL-10的产生是Treg细胞的抑制机制之一。然而，IL-10对Treg细胞本身的作用还不够清楚。在这项研究中，通过使用日本血吸虫感染的小鼠模型，我们发现升高的IL-10有助于Treg细胞的诱导，但削弱了它们的免疫抑制功能。我们的研究进一步表明，这可能与日本血吸虫感染过程中IL-10上调血清转化生长因子-1水平，减少膜结合的转化生长因子-1有关。此外，在哮喘小鼠模型中也证实了类似的IL-10对Treg细胞的调节作用。总体而言，我们的发现确定了先前未知的IL-10对Treg细胞的相反调节，并为免疫反应中的精确调节提供了深入的见解。
CD4(+) CD25(+) Foxp3(+) regulatory T (Treg) cells play an important role in maintaining immune homeostasis. Interleukin-10 (IL-10), a cytokine with anti-inflammatory capacities, also has a critical role in controlling immune responses. In addition, it is well known that production of IL-10 is one of the suppression mechanisms of Treg cells. However, the action of IL-10 on Treg cells themselves remains insufficiently understood. In this study, by using a Schistosoma japonicum-infected murine model, we show that the elevated IL-10 contributed to Treg cell induction but impaired their immunosuppressive function. Our investigations further suggest that this may relate to the up-regulation of serum transforming growth factor (TGF-) level but the decrease in membrane-bound TGF- of Treg cells by IL-10 during S. japonicum infection. In addition, similar IL-10-mediated regulation on Treg cells was also confirmed in the murine model of asthma. In general, our findings identify a previously unrecognized opposing regulation of IL-10 on Treg cells and provide a deep insight into the precise regulation in immune responses.