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调节性T细胞疗法通过减少IL-2促进TGF-β和IL-6依赖的炎症前的Th17细胞生成

Hao Cheng^1,2, Fang Nan^1,2, Ning Ji³

¹Department of Biotherapy, State Key Laboratory of Biotherapy and Cancer Center, Collaborative Innovation Center of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, China.

Nature communications

|August 16, 2025

概括

调节性T细胞疗法对自身免疫性疾病有希望,但可以促进致病性Th17细胞. 阻止IL-6/STAT3信号传递可以逆转这种情况,增强治疗潜力.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

CD4+Foxp3+调节性T细胞 (Tregs) 对免疫耐受性和预防炎症至关重要.
研究Tregs用于治疗自身免疫性疾病和移植与宿主疾病 (GvHD).
对Treg疗法的临床应用面临重大挑战.

研究的目的:

调查采用Treg疗法对致病性T助手17 (Th17) 细胞分化的影响.
阐明Tregs影响Th17细胞两极化的机制.
确定提高Treg基疗法的疗效的策略.

主要方法:

炎症性肠病 (IBD) 和实验性自身免疫脑膜炎 (EAE) 的小鼠模型.
对T细胞分化,细胞因子分泌 (IL-2,IL-6,TGF-β) 和信号通路 (STAT3,STAT5) 的分析.
对IL-6/STAT3信号通路的药理学阻断.

主要成果:

在IBD和EAE模型中,采用Treg疗法促进了IL-6和TGF-β依赖的致病性Th17细胞分化.
通过抑制和消耗IL-2,促进Th17分化,Tregs增加了效应T细胞中的p-STAT3/p-STAT5比率.
缺少IL-2信号增强了Th17细胞的炎症性质.
阻断IL-6/STAT3信号反转了致病性Th17分化,并改善了Treg治疗的疗效.

结论:

通过IL-2和IL-6/STAT3信号传递,Treg疗法可以无意中促进致病的Th17细胞.
向IL-6/STAT3通路可以克服这一局限性,并提高Treg治疗结果.
这些发现为推进免疫媒介疾病的临床Treg治疗提供了潜在的策略.

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