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(非)独自在家:屏障组织中的抗原呈递细胞 - T 细胞通讯。

(Not) Home alone: Antigen presenting cell - T Cell communication in barrier tissues.

机构信息

Department of Dermatology, Medical University of Vienna, Vienna, Austria.

CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.

出版信息

Front Immunol. 2022 Sep 29;13:984356. doi: 10.3389/fimmu.2022.984356. eCollection 2022.

DOI:10.3389/fimmu.2022.984356
PMID:36248804
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9556809/
Abstract

Priming of T cells by antigen presenting cells (APCs) is essential for T cell fate decisions, enabling T cells to migrate to specific tissues to exert their effector functions. Previously, these interactions were mainly explored using blood-derived cells or animal models. With great advances in single cell RNA-sequencing techniques enabling analysis of tissue-derived cells, it has become clear that subsets of APCs are responsible for priming and modulating heterogeneous T cell effector responses in different tissues. This composition of APCs and T cells in tissues is essential for maintaining homeostasis and is known to be skewed in infection and inflammation, leading to pathological T cell responses. This review highlights the commonalities and differences of T cell priming and subsequent effector function in multiple barrier tissues such as the skin, intestine and female reproductive tract. Further, we provide an overview of how this process is altered during tissue-specific infections which are known to cause chronic inflammation and how this knowledge could be harnessed to modify T cell responses in barrier tissue.

摘要

抗原呈递细胞 (APCs) 对 T 细胞的启动对于 T 细胞命运的决定至关重要,使 T 细胞能够迁移到特定组织发挥其效应功能。以前,这些相互作用主要是使用血液来源的细胞或动物模型来探索的。随着单细胞 RNA 测序技术的巨大进步,能够分析组织来源的细胞,人们已经清楚地认识到,APCs 的亚群负责在不同组织中启动和调节异质性 T 细胞效应反应。组织中 APC 和 T 细胞的这种组成对于维持体内平衡至关重要,并且已知在感染和炎症中会发生倾斜,导致病理性 T 细胞反应。本综述强调了皮肤、肠道和女性生殖道等多种屏障组织中 T 细胞启动和随后效应功能的共性和差异。此外,我们还概述了在已知引起慢性炎症的组织特异性感染过程中,这一过程是如何改变的,以及如何利用这些知识来调节屏障组织中的 T 细胞反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3082/9556809/cf800b040027/fimmu-13-984356-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3082/9556809/1d29538e1590/fimmu-13-984356-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3082/9556809/cd1a553ce45f/fimmu-13-984356-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3082/9556809/c15dada3ee2d/fimmu-13-984356-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3082/9556809/6ea24de99216/fimmu-13-984356-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3082/9556809/cf800b040027/fimmu-13-984356-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3082/9556809/1d29538e1590/fimmu-13-984356-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3082/9556809/cd1a553ce45f/fimmu-13-984356-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3082/9556809/c15dada3ee2d/fimmu-13-984356-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3082/9556809/6ea24de99216/fimmu-13-984356-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3082/9556809/cf800b040027/fimmu-13-984356-g005.jpg

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