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CD4⁺ T 细胞相关的细胞因子诱导了诱导多能干细胞衍生中脑天体细胞中的慢性亲炎性表型

Adina N MacMahon Copas^1,2, Sarah F McComish^1,2, Andreea Petrasca³

¹Discipline of Physiology, School of Medicine, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.

|July 26, 2024

概括

周围免疫细胞通过分泌细胞因子来影响帕金森病 (PD),这些细胞因子会激活中脑天体细胞. 这些细胞因子,就像IL-17A和TNF-α一样,协同增加了天体细胞的反应性,从而导致PD神经炎症.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

星球细胞对于大脑平衡至关重要,但在帕金森病 (PD) 中可以促进神经炎症.
越来越多地认识到外围免疫细胞参与PD病变的发生.
了解外周免疫因素如何影响神经细胞等中枢神经系统细胞对于PD研究至关重要.

研究的目的:

为了研究外周免疫分泌细胞因子对中脑天体细胞反应性的影响.
确定CD4+T细胞受条件介质 (CD4CM) 和特定细胞因子 (IL-17A,TNF-α) 对星球细胞炎症反应的影响.
评估IL-17A和TNF-α对天体细胞激活的潜在协同作用.

主要方法:

人类诱导的多能干细胞 (iPSC) 衍生的中脑天体细胞被培养.
在急性和慢性评估 (24小时,72小时,7天) 中,星球细胞暴露于不同度的CD4CM.
星球细胞被单独和组合地用IL-17A和TNF-α治疗,以评估协同的炎症反应.

主要成果:

CD4CM诱导了星细胞炎症基因表达和细胞因子释放的显著急性和慢性变化.
一种IL-17A和TNF-α的组合显示出对炎症基因表达和细胞因子释放的协同作用.
观察到IL-17A和TNF-α对天体细胞形态,DNA损伤标记物 (γH2AX) 和细胞死亡 (LDH释放) 的协同效应.

结论:

周围免疫分泌的细胞因子,特别是IL-17A和TNF-α,显著提高中脑星细胞的反应性.
IL-17A和TNF-α协同作用,调节星球细胞炎症状态,反映CD4CM的影响.
这些发现强调了外周免疫在调节天体细胞行为的关键作用,并可能导致PD的发病.

关键词:

帕金森病的疾病.星球细胞是星球细胞.细胞因子细胞因子诱导多能干细胞的诱导干细胞.神经炎症是一种神经炎症.反应性星球细胞的反应性星球细胞.

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