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经典树突状细胞中的干扰素基因刺激因子控制黏膜Th17对环二核苷酸的反应,以抵御肠道微生物感染,保护宿主。

Stimulator of Interferon Genes in Classical Dendritic Cells Controls Mucosal Th17 Responses to Cyclic Dinucleotides for Host Defenses Against Microbial Infections in Gut.

作者信息

Liu Song, Xia Qiuyuan, Wu Xiuwen, Sun Feng, Hu Qiongyuan, Wu Jie, Wang Meng, Rao Qiu, Guan Wenxian

机构信息

Department of General Surgery, Nanjing Drum Tower Hospital, Nanjing, China.

School of Medicine, Nanjing University, Nanjing, China.

出版信息

Front Immunol. 2018 May 16;9:1085. doi: 10.3389/fimmu.2018.01085. eCollection 2018.

DOI:10.3389/fimmu.2018.01085
PMID:29868030
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5964311/
Abstract

Cyclic dinucleotides are bacterial signal transducers that bind to host intracellular protein, stimulator of interferon genes (STING) encoded by . In this study, we demonstrate that STING triggers adaptive immune responses that control Th17 differentiation. Cyclic dinucleotides recognition enables classical dendritic cells (cDCs) that predominantly express CD103 to induce Th17 lymphocytes in an IL-6/IL-1β-dependent manner in gut. STING expression in human lamina propria is associated with the severity of mucosal inflammation and clinical disease activity in patients with Crohn's disease. Mice deficient in fail to mount Th17 responses to cyclic dinucleotides or prevent immune evasion of enteroinvasive pathogens. In summary, STING in mucosal cDCs controls Th17 subspecification that is essential for host defenses against microbial infection in gut-associated immune system.

摘要

环二核苷酸是细菌信号转导分子,可与宿主细胞内由……编码的蛋白质——干扰素基因刺激因子(STING)结合。在本研究中,我们证明STING触发适应性免疫反应,控制Th17细胞分化。环二核苷酸识别使主要表达CD103的经典树突状细胞(cDCs)能够以IL-6/IL-1β依赖的方式在肠道中诱导Th17淋巴细胞。人类固有层中STING的表达与克罗恩病患者黏膜炎症的严重程度和临床疾病活动相关。缺乏……的小鼠无法对环二核苷酸产生Th17反应,也无法防止肠道侵袭性病原体的免疫逃逸。总之,黏膜cDCs中的STING控制Th17亚群分化,这对于肠道相关免疫系统中宿主抵御微生物感染至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42f9/5964311/0ce7e629658d/fimmu-09-01085-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42f9/5964311/8e86d9c634a2/fimmu-09-01085-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42f9/5964311/af2749b8a772/fimmu-09-01085-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42f9/5964311/71ef131924a9/fimmu-09-01085-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42f9/5964311/49ecc62a982e/fimmu-09-01085-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42f9/5964311/0ce7e629658d/fimmu-09-01085-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42f9/5964311/8e86d9c634a2/fimmu-09-01085-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42f9/5964311/af2749b8a772/fimmu-09-01085-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42f9/5964311/71ef131924a9/fimmu-09-01085-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42f9/5964311/49ecc62a982e/fimmu-09-01085-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42f9/5964311/0ce7e629658d/fimmu-09-01085-g005.jpg

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本文引用的文献

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Signalling strength determines proapoptotic functions of STING.信号强度决定了STING的促凋亡功能。
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Human genetic variation and the gut microbiome in disease.人类遗传变异与疾病中的肠道微生物组。
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