Insulin-Like Growth Factors Are Key Regulators of T Helper 17 ...
2020年4月14日 · Disruption of Th17-Treg cell balance is implicated in a number of immune-mediated diseases, many of which display dysregulation of the insulin-like growth factor (IGF) …
Insulin-Like Growth Factors Are Key Regulators of T Helper 17 ...
2020年4月14日 · Disruption of Th17-Treg cell balance is implicated in a number of immune-mediated diseases, many of which display dysregulation of the insulin-like growth factor (IGF) …
Insulin and IGF-1 have both overlapping and distinct effects on CD4
2024年2月21日 · Given our findings that IGF-1R is significantly upregulated on Th17 cells compared to other CD4 + T helper subsets (Fig. 1e–f), and treatment with IGF-1 causes an …
Disruption of Th17-Treg cell bal-ance is implicated in a number of immune-mediated diseases, many of which display dysregulation of the insulin-like growth factor (IGF) system. Here, we …
The critical roles of IGFs in immune modulation and inflammation
2024年11月1日 · IGFs regulate T cell development, function, and balance between Th17 and Tregs. IGFs provide new therapeutic targets for treating inflammatory diseases and cancer. …
胰岛素样生长因子调控Th17与Treg细胞的平衡 - 科学网
2020年4月14日 · 美国阿拉巴马大学伯明翰分校Casey T. Weaver研究团队的一项最新研究显示，自身免疫反应中胰岛素样生长因子（IGF）是辅助性T细胞17（Th17）调节T细胞 ...
The ultimate microbial composition for correcting Th17/Treg cell ...
2025年1月10日 · Exogenous Th17 cells upregulate TGF-β to promote the upregulation of the surface marker molecule Foxp 3 in Treg cells and inhibit the expression of IL-23R in Th17 …
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21日，清华大学免疫学研究所董晨院士团队在Cell Press细胞出版社期刊Immunity上发表题为“The conserved non-coding sequences CNS6 and CNS9 control cytokine-induced …
Intricacies of TGF-β signaling in Treg and Th17 cell biology
2023年5月23日 · Here, we introduce the fundamental biology of TGF-β superfamily signaling, Treg cells, and Th17 cells and discuss in detail how the TGF-β superfamily contributes to Treg …
IGF-1R signalling contributes to IL-6 production and T cell ... - PubMed
Inhibition of IGF-1R on the level of insulin receptor substrates alleviates arthritis by restricting IL6-dependent formation of Th17 cells and may open for new treatment strategies in RA.