IL-6: regulator of Treg/Th17 balance - PubMed
IL-6 induces the development of Th17 cells from naïve T cells together with TGF-beta; in contrast, IL-6 inhibits TGF-beta-induced Treg differentiation. Dysregulation or overproduction of IL-6 …
总结 | Th17细胞必会知识点 - 知乎
IL-6或IL-1在TGFβ存在时诱导了STAT3信号和RORγt上调后，Naive CD4+T细胞开始向Th17谱系分化。 IL-21以自分泌的方式维持Th17分化，而来自抗原呈递细胞的IL-23促进Th17成熟、存活 …
TH17 cells require ongoing classic IL-6 receptor signaling to retain ...
Classic IL-6 receptor signaling was dominant over IL-6 trans-signaling in the colon because of the high levels of IL-6 produced there. Our findings establish that ongoing IL-6 is required for …
Th17 Cells Require Ongoing Classic IL-6 Receptor Signaling to …
Classic IL-6 receptor signaling was dominant over IL-6 trans -signaling in the colon due to the high levels of IL-6 produced there. Our findings establish that ongoing IL-6 is required for …
IL-6 programs TH-17 cell differentiation by promoting sequential ...
2007年6月20日 · We demonstrate here that IL-6 induced expression of IL-21 that amplified an autocrine loop to induce more IL-21 and IL-23 receptor in naive CD4 + T cells. Both IL-21 and …
Th17细胞概述-Th17细胞分化-赛默飞 | Thermo Fisher Scientific - CN
IL-6和IL-21通过STAT3信号促进Th17转录调节因子的表达，从而使CD4 + T细胞定向分化为Th17谱系。 STAT3信号通路的缺陷与IL-23R、关键Th17相关转录因子和效应细胞因子（如IL-17A …
董晨院士团队Immunity：细胞因子启动Th17细胞分化的新机制_澎 …
2020年8月30日 · 实验分析表明，CNS6或者CNS9缺失，并不影响RORγt阳性先天性免疫细胞亚群的功能和发育，但却导致了RORγt阳性CD4+ T细胞（即Th17细胞和Tr17细胞）的分化缺陷,以 …
TGF-β and IL-6 drive the production of IL-17 and IL-10 by T
2007年11月11日 · Studies have shown that transforming growth factor-β (TGF-β) and interleukin 6 (IL-6) are required for the lineage commitment of pathogenic IL-17-producing T helper cells …
IL-6 activates pathologic Th17 cell via STAT 3 phosphorylation in ...
2022年9月10日 · Cells producing both interferon-gamma (IFN-γ) and interleukin (IL)-17 have been reported to be the main pathologic Th17 (pTh17) cells that induce inflammation at sites of joint. …
IL-17与Th17细胞：从免疫卫士到疾病靶点-MedSci.cn
2025年3月14日 · Th17细胞的命名源于其核心产物IL-17，而后续研究进一步明确了其分化路径：IL-6、TGF-β和IL-23等因子协同调控，驱动RORγt转录因子的表达，最终形成具有独特功能 …