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ILC2 Proliferated by IL-33 Stimulation Alleviates Acute Colitis in Rag1-/- Mouse through Promoting M2 Macrophage Polarization.
Journal of Immunology Research ( IF 4.1 ) Pub Date : 2020-06-25 , DOI: 10.1155/2020/5018975
Yong You 1 , Xiaoqing Zhang 1 , Xiao Wang 1 , Dan Yue 1, 2 , Fanxiang Meng 1 , Junfeng Zhu 3 , Yuanyuan Wang 4 , Xun Sun 1
Affiliation  

This study was to identify functions of ILC2, a newly found innate lymphoid cell which mainly locates in mucosa organs like lungs and intestines, in IBD. We injected rIL-33 protein to C57/BL6 mouse to explore how IL-33 induces ILC2 proliferation. The results showed that ILC2 reached a proliferation peak at day 5 and expressed multiple surface markers like CD127, C-kit, CD69, CD44, ST2, CD27, DR3, MHCII, and CD90.2. ILC2 also expressed high quantity of IL-13 and IL-5 and few IL-17A which indicates a potentially immunological function in IBD development. Afterwards, we transferred sort purified ILC2 to Rag1-/- mouse given DSS to induce acute colitis in order to explore the innate function of ILC2. Data showed that ILC2 alleviates DSS-induced acute innate colitis by repairing epithelial barrier and restore body weight. Furthermore, we found that ILC2 can cause macrophages polarizing to M2 macrophages in the gut. Therefore, we concluded that ILC2 played a therapeutic role in mouse acute colitis.

中文翻译:

通过促进M2巨噬细胞极化,IL-33刺激的ILC2增殖可减轻Rag1-/-小鼠的急性结肠炎。

这项研究旨在鉴定ILC2的功能,ILC2是一种新发现的先天性淋巴样细胞,主要位于IBD中的粘膜器官(如肺和肠)中。我们向C57 / BL6小鼠注射了rIL-33蛋白,以探索IL-33如何诱导ILC2增殖。结果表明,ILC2在第5天达到增殖峰,并表达多种表面标记,如CD127,C-kit,CD69,CD44,ST2,CD27,DR3,MHCII和CD90.2。ILC2还表达大量的IL-13和IL-5,很少表达IL-17A,这表明IBD发育具有潜在的免疫功能。之后,我们将经过分类的纯化ILC2转移到Rag1 -/-为了探索ILC2的先天功能,给小鼠DSS诱导急性结肠炎。数据显示,ILC2通过修复上皮屏障并恢复体重减轻了DSS诱导的急性先天性结肠炎。此外,我们发现ILC2可导致巨噬细胞极化至肠道中的M2巨噬细胞。因此,我们得出结论,ILC2在小鼠急性结肠炎中具有治疗作用。
更新日期:2020-06-25
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