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PPARδ通过限制CIITA-MHC II表达来抑制内Tregs的抑制功能

Qiyuan Yang¹, Yuqiong Liang¹, Tomoko Inoue-Hatanaka¹

¹NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, CA, USA.

bioRxiv : the preprint server for biology

|January 7, 2025

概括

调控性T细胞 (Treg) 抑制抗瘤免疫力. 在Treg细胞中的PPARδ缺乏通过CIITA-MHC II增强免疫抑制,提供了一个新的癌症治疗点.

科学领域:

免疫学免疫学免疫学
癌症生物学癌症生物学
分子生物学分子生物学

背景情况:

调节性T (Treg) 细胞在抑制抗瘤免疫力方面至关重要,导致癌症结果不佳.
系统性Treg耗尽可能导致自身免疫,需要针对性的Treg特异性疗法.
了解瘤微环境 (TME) 中的Treg机制是新型癌症治疗的关键.

研究的目的:

为了研究氧酶增殖器激活受体β/δ (PPARδ) 在Treg细胞功能中的TME.内作用.
为了确定影响抗瘤免疫力的Treg细胞中PPARδ调节的下游途径.
探索针对癌症治疗的PPARδ调节通路的潜力.

主要方法:

在Treg细胞中的PPARδ剥离.
与抗原呈现相关的基因表达的分析 (CIITA,MHC II).
在体外测试以评估Treg抑制能力和细胞相互作用.
对1型干扰素信号通路 (JAK3,pSTAT1) 的研究.

主要成果:

在Treg细胞中的PPARδ缺乏会增加瘤生长和TME免疫抑制.
在Treg细胞中没有PPARδ上调的CIITA和MHC II表达.
缺乏PPARδ的Treg细胞,缺乏CIITA,通过抗原独立的Treg-MHC II和Tconv-TCR/CD4/Lag3相互作用增强了抗瘤反应.
1型干扰素信号,由PPARδ缺乏放大,驱动Treg细胞上的MHC II表达.

结论:

通过CIITA-MHC II通路,PPARδ信号调节Treg细胞在TME中的适应和抑制功能.
向MHC II+ Treg细胞是一个有希望的策略,可以增强抗瘤免疫力,同时减轻自身免疫副作用.
CIITA 作为 Treg 细胞中 PPARδ 的关键下游介质.

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