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在大肠炎小鼠中,TRAF5通过Runx1调节肠粘膜Th1/Th17细胞的免疫反应

Mengting Li^1,2, Caiqin Gan^1,2, Runan Zhang^1,2

¹Department of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, China.

|August 14, 2023

概括

瘤亡因子相关因子5 (TRAF5) 缺乏症通过通过Runx1.1.促进Th1和Th17细胞分化而加剧炎症性肠病 (IBD). 在CD4+T细胞中准TRAF5为IBD提供了潜在的新疗法.

科学领域:

免疫学免疫学免疫学
胃肠病学胃肠病学
分子生物学分子生物学

背景情况:

炎症性肠病 (IBD) 涉及CD4+ T助手1 (Th1) 和T助手17 (Th17) 细胞的反应.
瘤坏死因子相关因子5 (TRAF5) 缺乏会使结肠炎恶化,但其在IBD病原发生中的作用尚不清楚.

研究的目的:

研究TRAF5在调节IBD病原体中的CD4+T细胞免疫反应中的作用.
阐明TRAF5在结肠炎中影响Th1和Th17细胞分化的机制.

主要方法:

在Rag2-/-小鼠中建立了一种慢性结肠炎模型,使用T细胞从TRAF5-/-或野生型 (WT) CD4+CD45RB高T细胞转移.
在体内利用腺相关病毒 (AAV) 介导的基因淘汰来抑制子相关转录因子1 (Runx1).
使用RT-PCR,免疫组织化学,ELISA和流细胞计量量化Th1和Th17细胞细胞因子 (INF-γ,TNF-α,IL-17a).

主要成果:

与WT对照组相比,TRAF5-/- CD4+ T细胞诱导了更严重的肠道炎症,并增加了INF-γ,TNF-α和IL-17a的表达.
流细胞测量显示,在接受TRAF5-/- T细胞的小鼠的肠粘膜中,INF-γ+,IL-17a+和INF-γ+IL-17a+ CD4+ T细胞的百分比明显更高.
在大肠炎模型中,Runx1淘汰赛抑制了TRAF5-/- CD4+ T细胞分化为Th1和Th17细胞.

结论:

TRAF5通过Runx1调节Th1和Th17细胞分化和免疫反应,从而导致大肠炎的发病.
在CD4+T细胞中准TRAF5代表了IBD的潜在新疗法策略.

关键词:

转移T细胞的大肠炎在TRAF5中,TRAF5是指TRAF5.在 Th1 细胞中.在Th17细胞中.炎症性肠病是一种炎症性肠病.

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