Helminth‐induced regulation of T‐cell transfer colitis requires intact and regulated T cell Stat6 signaling in mice,European Journal of Immunology

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Helminth‐induced regulation of T‐cell transfer colitis requires intact and regulated T cell Stat6 signaling in mice
European Journal of Immunology ( IF 4.5 ) Pub Date : 2020-10-16 , DOI: 10.1002/eji.201848072
Ahmed Metwali _{1,

2} , Sarah Winckler _{1,

2} , Joseph F. Urban ₃ , Mark H. Kaplan ₄ , M. Nedim Ince _{1,

2} , David E. Elliott _{1,

2}

Affiliation

Infection with parasitic worms (helminths) alters host immune responses and can inhibit pathogenic inflammation. Helminth infection promotes a strong Th2 and T regulatory response while suppressing Th1 and Th17 function. Th2 responses are largely dependent on transcriptional programs directed by Stat6‐signaling. We examined the importance of intact T cell Stat6 signaling on helminth‐induced suppression of murine colitis that results from T cell transfer into immune‐deficient mice. Colonization with the intestinal nematode Heligmosomoides polygyrus bakeri resolves WT T cell transfer colitis. However, if the transferred T cells lack intact Stat6 then helminth exposure failed to attenuate colitis or suppress MLN T cell IFN‐γ or IL17 production. Loss of Stat6 signaling resulted in decreased IL10 and increased IFN‐γ co‐expression by IL‐17⁺ T cells. We also transferred T cells from mice with constitutive T cell expression of activated Stat6 (Stat6VT). These mice developed a severe eosinophilic colitis that also was not attenuated by helminth infection. These results show that T cell expression of intact but regulated Stat6 signaling is required for helminth infection‐associated regulation of pathogenic intestinal inflammation.

中文翻译：

蠕虫诱导的T细胞转移性结肠炎的调节需要小鼠中完整且受调节的T细胞Stat6信号传导

寄生虫（蠕虫）感染会改变宿主的免疫反应，并能抑制致病性炎症。蠕虫感染可促进Th2和T的强烈调节反应，同时抑制Th1和Th17的功能。Th2反应很大程度上取决于Stat6信号转导指导的转录程序。我们研究了完整的T细胞Stat6信号传导对蠕虫诱导的鼠结肠炎抑制的重要性，这种抑制是由T细胞转移到免疫缺陷小鼠中引起的。肠道线虫Heligmosomoides polygyrus bakeri的定殖解决WT T细胞转移性结肠炎。但是，如果转移的T细胞缺乏完整的Stat6，则蠕虫暴露不能减轻结肠炎或抑制MLN T细胞IFN-γ或IL17的产生。Stat6信号的丧失导致IL-17 ⁺ T细胞的IL10降低和IFN-γ共表达增加。我们还从具有激活的Stat6（Stat6VT）的组成性T细胞表达的小鼠中转移了T细胞。这些小鼠发展成严重的嗜酸性结肠炎，蠕虫感染也不能减弱这种嗜酸性结肠炎。这些结果表明，蠕虫感染相关的病原性肠道炎症调节需要完整但受调节的Stat6信号传导的T细胞表达。

更新日期：2020-10-16

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