Here, we showed that anti-inflammatory interleukin-10 (IL-10), and not pro-inflammatory IL-6 and IL-23 cytokine signaling, endowed Treg cells with the ability to suppress pathogenic Th17 cell responses.

利用最新的细胞分选技术，研究团队将产生IL-10的Treg细胞分选出来，对IL-10+FOXP3+Treg细胞的转录组学和功能标志物进行了分析，并在体外和体内证明IL-10+ FOXP3+Treg细胞具有更强的免疫抑制功能。

2016年4月14日 · Regulatory T cells (Tregs) expand in peripheral lymphoid organs and can produce immunosuppressive cytokines to support tumor growth. IL-10 abrogation efficiently induces Treg formation but...

2015年10月15日 · In this article, we show that the presence of IL-10, in addition to TGF-β, leads to increased expansion of Foxp3 (+) iTregs with enhanced CTLA-4 expression and suppressive capability, comparable to that of natural Tregs.

2015年10月15日 · In this article, we show that the presence of IL-10, in addition to TGF-β, leads to increased expansion of Foxp3 + iTregs with enhanced CTLA-4 expression and suppressive capability, comparable to that of natural Tregs.

2007年8月12日 · CD4 + regulatory T cells (T reg cells) that produce interleukin 10 (IL-10) are important contributors to immune homeostasis. We generated mice with a 'dual-reporter' system of the genes...

2015年9月11日 · 尽管众所周知 IL-10 是 Treg 抑制的重要介质，但 IL-10 对 Treg 本身的作用还不太清楚。 在本文中，我们表明，除了 TGF-β 外，IL-10 的存在会导致 Foxp3+ iTreg 的扩增增加，CTLA-4 表达和抑制能力增强，与天然 Treg 相当。

2013年10月8日 · In this study, we investigated the origin and function of IL-10–producing cells in the tumor microenvironment using transplantable tumor models in mice. The majority of tumor-associated IL-10 was produced by an activated Treg population. IL-10 production by Tregs was required to restrain Th17-type inflammation.

2008年4月11日 · To directly investigate a role for IL-10 in Treg cell-mediated suppression, we generated Foxp3 YFP-Cre mice, capable of Treg cell-specific inactivation of genes of interest, and crossed them with Il10 flox/flox mice harboring a conditional Il10 allele. We found that the selective disruption of IL-10 expression in Treg cells led to spontaneous ...

Here, we found that the cytokines IL-10 and IL-35 (Ebi3-IL-12α heterodimer) were divergently expressed by T reg cell subpopulations in the tumor microenvironment (TME) and cooperatively promoted intratumoral T cell exhaustion by modulating several inhibitory receptor expression and exhaustion-associated transcriptomic signature of CD8 + TILs.