Nat Commun:花生四烯酸调节类风湿关节炎患者T细胞的钙信号传导促进滑膜炎的发生

2021-02-18 xiaozeng MedSci原创

类风湿关节炎(RA)和银屑病关节炎(PsA)是全身性自身免疫性疾病,其表现为慢性滑膜炎,可导致关节结构的破坏。

类风湿关节炎(RA)和银屑病关节炎(PsA)是全身性自身免疫性疾病,其表现为慢性滑膜炎,可导致关节结构的破坏。PsA发生在牛皮癣的环境中,牛皮癣作为一种自身免疫性皮肤病,其特征是由于皮肤发炎导致的表皮层过度快速生长。

两种疾病的共同点是CD4+T细胞的反应异常与疾病的发病机制相关。既往研究显示,RA的许多遗传易感因素与T细胞的功能有关,同样的,PsA的疾病易感基因经常参与T细胞的生物功能。


虽然在RA和PsA中已发现T细胞的分化异常,但目前尚不清楚促进自身反应性T细胞激活的相关分子机制。

RA CD4+T细胞中Ca2+通道蛋白ORAI3的表达水平升高

在该研究中,研究人员发现,RA和PsA患者的CD4+T细胞中钙通道蛋白ORAI3的表达水平升高,提高花生四烯酸(Arachidonic acid)调节钙选择性通道(ARC)的活性并使T细胞对花生四烯酸致敏。而在系统性红斑狼疮患者的T细胞中并未发生类似的表达升高现象。


进一步的研究显示,RA和PsA T细胞中ORAI3转录水平的升高是由IKAROS的表达降低所引起的,而IKAROS是ORAI3启动子转录的阻遏因子。通过花生四烯酸刺激ARC通道激活不仅能够引起钙内流,且会引起T细胞受体信号转导级联反应相关蛋白的磷酸化。

花生四烯酸通过介导ORAI3激活T细胞

在人类滑膜嵌合小鼠模型中,沉默来自RA患者的过继转移性T细胞中的ORAI3可减轻组织炎症反应,而降低来自健康个体的过继T细胞中IKAROS的表达水平则会诱导滑膜炎。


总而言之,该研究结果发现,IKAROS表达水平降低诱导的ARC活性升高会使得T细胞更具反应性,并最终导致RA和PsA中慢性炎症的发生


原始出处:

Ye, Z., Shen, Y., Jin, K. et al. Arachidonic acid-regulated calcium signaling in T cells from patients with rheumatoid arthritis promotes synovial inflammation. Nat Commun 12, 907 (10 February 2021).

 

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    2021-02-20 lmm397
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    2021-02-20 pcw106
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