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黏膜相关共生菌群驱动 IBD 来源的肠道 iNKT 细胞发挥致病功能。

Mucosa-associated microbiota drives pathogenic functions in IBD-derived intestinal iNKT cells.

机构信息

Department of Experimental Oncology, IEO, European Istitute of Oncology IRCCS, Milan, Italy.

Gastroenterology and Endoscopy Unit, Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico, Milan, Italy.

出版信息

Life Sci Alliance. 2019 Feb 13;2(1). doi: 10.26508/lsa.201800229. Print 2019 Feb.

DOI:10.26508/lsa.201800229
PMID:30760554
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6374994/
Abstract

Inflammatory bowel disease (IBD) pathogenesis has been linked to the aberrant activation of the Gut-associated lymphoid tissues against components of the intestinal microbiota. Although the contribution of CD4 T helper cells to inflammatory processes is being increasingly acknowledged, the functional engagement of human invariant natural killer T (iNKT) cells is still poorly defined. Here, we evaluated the functional characteristics of intestinal iNKT cells during IBD pathogenesis and to exploit the role of mucosa-associated microbiota recognition in triggering iNKT cells' pro-inflammatory responses in vivo. Lamina propria iNKT cells, isolated from surgical specimens of active ulcerative colitis and Crohn's disease patients and non-IBD donors, were phenotypically and functionally analyzed ex vivo, and stable cell lines and clones were generated for in vitro functional assays. iNKT cells expressing a pro-inflammatory cytokine profile were enriched in the lamina propria of IBD patients, and their exposure to the mucosa-associated microbiota drives pro-inflammatory activation, inducing direct pathogenic activities against the epithelial barrier integrity. These observations suggest that iNKT cell pro-inflammatory functions may contribute to the fuelling of intestinal inflammation in IBD patients.

摘要

炎症性肠病（IBD）的发病机制与肠道微生物群成分对肠道相关淋巴组织的异常激活有关。尽管 CD4 T 辅助细胞对炎症过程的贡献越来越被承认，但人类不变自然杀伤 T（iNKT）细胞的功能参与仍未得到明确界定。在这里，我们评估了 IBD 发病过程中肠道 iNKT 细胞的功能特征，并利用黏膜相关微生物群识别在体内触发 iNKT 细胞促炎反应的作用。从活动性溃疡性结肠炎和克罗恩病患者及非 IBD 供体的手术标本中分离出黏膜固有层 iNKT 细胞，进行体外表型和功能分析，并生成稳定的细胞系和克隆进行体外功能测定。表达促炎细胞因子谱的 iNKT 细胞在 IBD 患者的固有层中富集，它们暴露于黏膜相关微生物群会导致促炎激活，诱导对上皮屏障完整性的直接致病活性。这些观察结果表明，iNKT 细胞的促炎功能可能有助于为 IBD 患者的肠道炎症提供燃料。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/022baf69eaac/LSA-2018-00229_FigS12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/339bd34ed9a9/LSA-2018-00229_FigS6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/8d533bb1d18a/LSA-2018-00229_FigS7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/f14b409adff6/LSA-2018-00229_Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/f8b949b8c9f7/LSA-2018-00229_Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/5fa887a679f9/LSA-2018-00229_FigS8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/9dcc0b7339fc/LSA-2018-00229_Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/d692440a1234/LSA-2018-00229_FigS9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/c5a73ce4681f/LSA-2018-00229_FigS10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/d52105da5629/LSA-2018-00229_Fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/aa3308057777/LSA-2018-00229_FigS11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/2a3c842c63d4/LSA-2018-00229_Fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/e71f71c610b5/LSA-2018-00229_Fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/022baf69eaac/LSA-2018-00229_FigS12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/339bd34ed9a9/LSA-2018-00229_FigS6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/8d533bb1d18a/LSA-2018-00229_FigS7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/f14b409adff6/LSA-2018-00229_Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/f8b949b8c9f7/LSA-2018-00229_Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/5fa887a679f9/LSA-2018-00229_FigS8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/9dcc0b7339fc/LSA-2018-00229_Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/d692440a1234/LSA-2018-00229_FigS9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/c5a73ce4681f/LSA-2018-00229_FigS10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/d52105da5629/LSA-2018-00229_Fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/aa3308057777/LSA-2018-00229_FigS11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/2a3c842c63d4/LSA-2018-00229_Fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/e71f71c610b5/LSA-2018-00229_Fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375f/6374994/022baf69eaac/LSA-2018-00229_FigS12.jpg

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