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抑制JAK2/STAT5通过调节T细胞极化来保护小鼠免受实验性自身免疫脑膜炎的影响

Yingying Wei¹, Zachary Braunstein², Jun Chen³

¹Department of Rheumatology and Immunology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China; Cardiovascular Research Institute, Case Western Reserve University, Cleveland, OH 44106, USA.

International immunopharmacology

|June 3, 2023

概括

在T细胞中的Janus酶2 (JAK2) 信号驱动多发性硬化症 (MS) 病原体. 在MS动物模型中,抑制JAK2有效降低了自身免疫反应和疾病活性.

科学领域:

免疫学免疫学免疫学
神经科学是一个神经科学.
药理学药理学是指药理学的学科.

背景情况:

多发性硬化症 (MS) 是一种自身免疫性疾病,主要影响T细胞.
在MS中控制T细胞反应的特定信号通路仍然不完全理解.
简氏激酶2 (JAK2) 对于免疫细胞中细胞因子受体信号传递至关重要.

研究的目的:

在MS的背景下调查JAK2在T细胞调节中的作用.
评估JAK2抑制在MS治疗中的治疗潜力.

主要方法:

使用可诱导的全身和T细胞特异性的JAK2淘汰赛小鼠模型.
在实验性自身免疫脑膜炎 (EAE) 中评估疾病发病,脱髓化和白细胞透.
分析了T辅助细胞分化 (TH1,TH17),IFNγ产生和STAT5酸化在体外和体内.
给EAE小鼠使用JAK1/2抑制剂巴里西提尼布和选择性JAK2抑制剂费德拉提尼布.

主要成果:

在T细胞中的JAK2缺乏完全阻止了EAE的发生,并减少了脊髓炎症和脱髓化.
破坏JAK2抑制了TH1分化和IFNγ产生,与减少STAT5酸化有关.
用巴里西提尼布或费德拉提尼布抑制JAK2,减弱了TH1/TH17频率和减轻了EAE疾病活性.

结论:

在T淋巴细胞中过度活跃的JAK2信号传递是EAE病变发生的关键驱动因素.
针对JAK2代表了对MS等自身免疫性疾病的有前途的治疗策略.

关键词:

实验性的自身免疫脑筋炎这就是JAK2的意思.多发性硬化症是多发性硬化症.在STAT5中,我们使用了STAT5.一个T细胞细胞.T(H) 1 一个

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