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由IL-4诱导的T_reg的数量和CTLA-4表达的减少,在严重的亚托皮性皮肤炎中损害了Th2型炎症的抑制

Bocheng Wang¹, Zhiying Yu¹, Jiao Liu²

¹The First School of Clinical Medicine, Southern Medical University, Guangzhou, China; Department of Dermatology, Dermatology Hospital, Southern Medical University, Guangzhou, China.

Journal of dermatological science

|March 31, 2024

概括

皮炎 (AD) 的高IL-4水平在表观遗传上降低了调节性T细胞 (Treg) 和CTLA-4表达,损害了免疫抑制. 阻止IL-4Rα信号传递可以恢复AD中的Treg功能.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
皮肤病学皮肤病学

背景情况:

调节性T细胞 (Treg) 对于免疫平衡和抑制Th2细胞反应至关重要.
在阿托皮性皮肤炎 (AD) 和Th2炎症中Treg功能障碍背后的分子机制尚未完全理解.

研究的目的:

阐明驱动AD中Treg细胞的定量和功能变化的分子机制.
调查IL-4在AD病变发生过程中的Treg细胞损伤中的作用.

主要方法:

使用流细胞计,mRNA测序,共同培养试验,共同免疫沉和染色体免疫沉.
采用了体外研究,AD小鼠模型和来自AD个体的患者样本.

主要成果:

在轻度/中度AD时,Treg细胞数量增加,但在严重AD时减少,与血清IL-4水平相关.
高水平的IL-4,通过IL-4/pSTAT6通路,招募DNMT1和HDAC2,抑制Foxp3和CTLA-4转录.
IL-4损害了Treg介导的Th2分化抑制;IL-4Rα阻断恢复了AD模型和患者的Treg数量和功能.

结论:

特雷格细胞数与AD严重程度和血清IL-4水平相关.
升高的IL-4在表观遗传上降低了AD中的Treg细胞数量和CTLA-4表达.
由于IL-4降低了Treg细胞上的CTLA-4,破坏了Th2细胞分化的抑制,导致AD病理.

关键词:

亚托邦性皮肤炎 (Atopic Dermatitis) 是一种不良的疾病.2型T-辅助细胞类型的细胞.表观遗传学是指表观遗传学.介质蛋白-4 介质蛋白-4 监管性T细胞监管性T细胞

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