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人类肠道单核吞噬细胞在健康和炎症性肠病中的作用。

Human Intestinal Mononuclear Phagocytes in Health and Inflammatory Bowel Disease.

机构信息

Department of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.

出版信息

Front Immunol. 2020 Mar 18;11:410. doi: 10.3389/fimmu.2020.00410. eCollection 2020.

DOI:10.3389/fimmu.2020.00410
PMID:32256490
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7093381/
Abstract

Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is a complex immune-mediated disease of the gastrointestinal tract that increases morbidity and negatively influences the quality of life. Intestinal mononuclear phagocytes (MNPs) have a crucial role in maintaining epithelial barrier integrity while controlling pathogen invasion by activating an appropriate immune response. However, in genetically predisposed individuals, uncontrolled immune activation to intestinal flora is thought to underlie the chronic mucosal inflammation that can ultimately result in IBD. Thus, MNPs are involved in fine-tuning mucosal immune system responsiveness and have a critical role in maintaining homeostasis or, potentially, the emergence of IBD. MNPs include monocytes, macrophages and dendritic cells, which are functionally diverse but highly complementary. Despite their crucial role in maintaining intestinal homeostasis, specific functions of human MNP subsets are poorly understood, especially during diseases such as IBD. Here we review the current understanding of MNP ontogeny, as well as the recently identified human intestinal MNP subsets, and discuss their role in health and IBD.

摘要

炎症性肠病(IBD),包括克罗恩病和溃疡性结肠炎,是一种复杂的免疫介导的胃肠道疾病,会增加发病率并对生活质量产生负面影响。肠道单核吞噬细胞(MNP)在维持上皮屏障完整性方面起着至关重要的作用,同时通过激活适当的免疫反应来控制病原体的入侵。然而,在遗传易感性个体中,对肠道菌群的失控免疫激活被认为是导致慢性黏膜炎症的基础,而慢性黏膜炎症最终可能导致 IBD。因此,MNP 参与了精细调节黏膜免疫系统的反应性,并在维持体内平衡或潜在的 IBD 发生中起着关键作用。MNP 包括单核细胞、巨噬细胞和树突状细胞,它们具有不同的功能,但高度互补。尽管它们在维持肠道内环境稳定方面起着至关重要的作用,但人类 MNP 亚群的特定功能仍知之甚少,特别是在 IBD 等疾病期间。在这里,我们综述了 MNP 发生发展的最新认识,以及最近鉴定的人类肠道 MNP 亚群,并讨论了它们在健康和 IBD 中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86b8/7093381/54cb332a1b0b/fimmu-11-00410-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86b8/7093381/e13906138849/fimmu-11-00410-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86b8/7093381/c54e49e5dab5/fimmu-11-00410-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86b8/7093381/4f1821c00963/fimmu-11-00410-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86b8/7093381/54cb332a1b0b/fimmu-11-00410-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86b8/7093381/e13906138849/fimmu-11-00410-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86b8/7093381/caef5dd4248f/fimmu-11-00410-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86b8/7093381/e1593ccc3967/fimmu-11-00410-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86b8/7093381/c54e49e5dab5/fimmu-11-00410-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86b8/7093381/4f1821c00963/fimmu-11-00410-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86b8/7093381/54cb332a1b0b/fimmu-11-00410-g0006.jpg

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