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本文引用的文献

1
Mucus Architecture and Near-Surface Swimming Affect Distinct Salmonella Typhimurium Infection Patterns along the Murine Intestinal Tract.黏液结构和近表面游泳行为影响鼠肠道中沙门氏菌 Typhimurium 感染的不同模式。
Cell Rep. 2019 May 28;27(9):2665-2678.e3. doi: 10.1016/j.celrep.2019.04.106.
2
Epithelial retinoic acid receptor β regulates serum amyloid A expression and vitamin A-dependent intestinal immunity.上皮细胞视黄酸受体 β 调节血清淀粉样蛋白 A 的表达和维生素 A 依赖性肠道免疫。
Proc Natl Acad Sci U S A. 2019 May 28;116(22):10911-10916. doi: 10.1073/pnas.1812069116. Epub 2019 May 16.
3
Comparison of Co-housing and Littermate Methods for Microbiota Standardization in Mouse Models.比较共住房和同窝仔方法对小鼠模型中微生物群标准化的影响。
Cell Rep. 2019 May 7;27(6):1910-1919.e2. doi: 10.1016/j.celrep.2019.04.023.
4
secreted antigen A generates muropeptides to enhance host immunity and limit bacterial pathogenesis.分泌抗原 A 产生肽聚糖以增强宿主免疫力并限制细菌发病机制。
Elife. 2019 Apr 10;8:e45343. doi: 10.7554/eLife.45343.
5
Intestinal Epithelial Cells and the Microbiome Undergo Swift Reprogramming at the Inception of Colonic Citrobacter rodentium Infection.肠道上皮细胞和微生物组在结肠柠檬酸杆菌感染开始时迅速重新编程。
mBio. 2019 Apr 2;10(2):e00062-19. doi: 10.1128/mBio.00062-19.
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Glucocorticoid Receptor-Deficient Foxp3 Regulatory T Cells Fail to Control Experimental Inflammatory Bowel Disease.糖皮质激素受体缺陷的 Foxp3 调节性 T 细胞无法控制实验性炎症性肠病。
Front Immunol. 2019 Mar 18;10:472. doi: 10.3389/fimmu.2019.00472. eCollection 2019.
7
The potential probiotic Lactobacillus rhamnosus CNCM I-3690 strain protects the intestinal barrier by stimulating both mucus production and cytoprotective response.潜在的益生菌鼠李糖乳杆菌 CNCM I-3690 菌株通过刺激黏液产生和细胞保护反应来保护肠道屏障。
Sci Rep. 2019 Apr 1;9(1):5398. doi: 10.1038/s41598-019-41738-5.
8
A Weaning Reaction to Microbiota Is Required for Resistance to Immunopathologies in the Adult.微生物群的断奶反应是成年后抵抗免疫病理学所必需的。
Immunity. 2019 May 21;50(5):1276-1288.e5. doi: 10.1016/j.immuni.2019.02.014. Epub 2019 Mar 19.
9
TLR9 limits enteric antimicrobial responses and promotes microbiota-based colonisation resistance during Citrobacter rodentium infection.TLR9 限制肠道抗菌反应并促进柠檬酸杆菌感染期间基于微生物组的定植抗性。
Cell Microbiol. 2019 Jul;21(7):e13026. doi: 10.1111/cmi.13026. Epub 2019 May 7.
10
Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis.抗共生 IgG 驱动溃疡性结肠炎的肠道炎症和 17 型免疫。
Immunity. 2019 Apr 16;50(4):1099-1114.e10. doi: 10.1016/j.immuni.2019.02.006. Epub 2019 Mar 12.

肠上皮细胞:位于微生物群和黏膜免疫的交界处。

Intestinal epithelial cells: at the interface of the microbiota and mucosal immunity.

机构信息

Cambridge Institute of Therapeutic Immunology & Infectious Disease, University of Cambridge, Cambridge, UK.

出版信息

Immunology. 2019 Dec;158(4):267-280. doi: 10.1111/imm.13117. Epub 2019 Oct 4.

DOI:10.1111/imm.13117
PMID:31509239
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6856932/
Abstract

The intestinal epithelium forms a barrier between the microbiota and the rest of the body. In addition, beyond acting as a physical barrier, the function of intestinal epithelial cells (IECs) in sensing and responding to microbial signals is increasingly appreciated and likely has numerous implications for the vast network of immune cells within and below the intestinal epithelium. IECs also respond to factors produced by immune cells, and these can regulate IEC barrier function, proliferation and differentiation, as well as influence the composition of the microbiota. The mechanisms involved in IEC-microbe-immune interactions, however, are not fully characterized. In this review, we explore the ability of IECs to direct intestinal homeostasis by orchestrating communication between intestinal microbes and mucosal innate and adaptive immune cells during physiological and inflammatory conditions. We focus primarily on the most recent findings and call attention to the numerous remaining unknowns regarding the complex crosstalk between IECs, the microbiota and intestinal immune cells.

摘要

肠上皮细胞在微生物群和身体其他部位之间形成一道屏障。此外,除了作为物理屏障发挥作用外,肠上皮细胞(IECs)在感知和响应微生物信号方面的功能越来越受到重视,这可能对肠上皮内和下方的大量免疫细胞网络产生诸多影响。IEC 还会对免疫细胞产生的因子做出反应,这些因子可以调节 IEC 屏障功能、增殖和分化,并影响微生物组的组成。然而,IEC-微生物-免疫相互作用的机制尚未完全阐明。在这篇综述中,我们探讨了 IEC 通过在生理和炎症条件下协调肠道微生物与黏膜固有和适应性免疫细胞之间的通讯,从而指导肠道稳态的能力。我们主要关注最近的发现,并提请注意 IEC、微生物组和肠道免疫细胞之间复杂的串扰仍存在许多未知。