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在自身免疫性神经炎症中,Pin1维持了致病性Th17细胞的效应器程序

Guangyue Fan¹, Guangliang Li², Long Li¹

¹Tianjin Institute of Immunology, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, State Key Laboratory of Experimental Hematology, Department of Immunology, Tianjin Medical University, Tianjin, 300070, China; Department of Pediatric Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300070, China.

Journal of autoimmunity

|June 4, 2024

概括

Pin1蛋白增强RORγt的活性,这是Th17细胞发育的关键因素,驱动诸如多发性硬化症 (MS) 等自身免疫性疾病. 抑制Pin1会减少Th17细胞和神经炎症,为MS提供潜在的治疗点.

科学领域:

免疫学免疫学免疫学
神经科学是一个神经科学.
分子生物学分子生物学

背景情况:

Th17细胞是自身免疫性疾病的核心,如多发性硬化症 (MS) 和实验性自身免疫性脑膜炎 (EAE).
转录因子RORγt对于Th17细胞发育和效应因子功能至关重要.
了解RORγt的调节机制对于开发向疗法至关重要.

研究的目的:

调查Peptidylprolyl Cis/Trans异构酶,NIMA交互1 (Pin1) 在EAE病变发生中的作用及其对MS的相关性.
阐明Pin1影响Th17细胞活动和RORγt功能的分子机制.
评估针对Pin1在自身免疫性炎症疾病中的治疗潜力.

主要方法:

在多发性硬化患者样本和EAE小鼠模型中分析Pin1表达.
使用转基因小鼠模型,细胞检测和分子生物学技术.
研究Pin1与STAT3和RORγt在Th17细胞中的相互作用.
评估Pin1抑制对EAE的影响 (遗传和药理学).

主要成果:

在MS患者和EAE小鼠的中枢神经系统中,Pin1表达升高.
Pin1促进了炎症部位的致病性Th17细胞的激活和效应器功能.
Pin1稳定了STAT3的酸化,并增强了RORγt的交换活化,维持了Th17细胞效应器程序.
抑制Pin1可以减少Th17细胞数量,神经炎症,并缓解EAE症状.

结论:

在EAE中,Pin1在维持致病性Th17细胞反应方面发挥着关键作用.
Pin1通过稳定STAT3酸化和增强RORγt活性而起作用.
向Pin1代表了对MS和其他自身免疫性疾病的有希望的治疗策略.

关键词:

实验性的自身免疫脑膜炎 (EAE)多发性硬化症 (MS) 是一种疾病.一个Pin1一个Pin1 罗尔特的时间.Th17 这是一个很好的方法.

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