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走向一种区分 FOXP3 调节性 T 细胞不同功能的范式。

Toward a Paradigm to Distinguish Distinct Functions of FOXP3 Regulatory T Cells.

机构信息

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL.

Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL.

出版信息

Immunohorizons. 2021 Dec 10;5(12):944-952. doi: 10.4049/immunohorizons.2100046.

DOI:10.4049/immunohorizons.2100046
PMID:34893512
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8691855/
Abstract

FOXP3 regulatory T (Treg) cells are a unique subset of CD4 T cells that classically function as master regulators of immune homeostasis. Besides this canonical suppressive role, which is required to maintain self-tolerance, a growing body of literature has identified Treg cells as critical orchestrators of tissue protection during acute stress and as effector cells that drive repair following tissue injury. Despite substantial interest in these distinct roles, the field has struggled to disentangle Treg cell suppressive functions from those that promote tissue defense and repair. In this article, we will examine the literature in the context of specific physiologic settings, contrasting the suppressive function of Treg cells with their emerging roles in promoting tissue homeostasis and tissue repair. Further, we will discuss a new paradigm differentiating tissue defense from tissue repair-a paradigm needed to translate Treg cell-based therapies to the clinic.

摘要

叉头框蛋白 P3 调节性 T(Treg)细胞是 CD4 T 细胞的一个独特亚群,其经典功能是作为免疫稳态的主要调节者。除了维持自身耐受所必需的经典抑制作用外,越来越多的文献已经确定 Treg 细胞是急性应激时组织保护的关键协调者,也是驱动组织损伤后修复的效应细胞。尽管人们对这些不同的作用有很大的兴趣,但该领域一直在努力将 Treg 细胞的抑制功能与其促进组织防御和修复的作用区分开来。在本文中,我们将根据特定的生理环境来检查文献,将 Treg 细胞的抑制功能与其在促进组织稳态和组织修复方面的新兴作用进行对比。此外,我们还将讨论一个新的范式,将组织防御与组织修复区分开来,这是将基于 Treg 细胞的治疗方法转化为临床应用所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5be8/8691855/6bc34dd4a9cc/nihms-1763981-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5be8/8691855/a10cfe7ea7fb/nihms-1763981-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5be8/8691855/6bc34dd4a9cc/nihms-1763981-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5be8/8691855/a10cfe7ea7fb/nihms-1763981-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5be8/8691855/6bc34dd4a9cc/nihms-1763981-f0002.jpg

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Notch4 signaling limits regulatory T-cell-mediated tissue repair and promotes severe lung inflammation in viral infections.Notch4 信号通路限制调节性 T 细胞介导的组织修复,并促进病毒感染中的严重肺部炎症。
Immunity. 2021 Jun 8;54(6):1186-1199.e7. doi: 10.1016/j.immuni.2021.04.002. Epub 2021 Apr 28.
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Single-cell chromatin accessibility landscape identifies tissue repair program in human regulatory T cells.
在恶性肿瘤和病毒性肺炎期间,AMPK对于调节性T细胞(Treg)功能适应微环境应激是必需的。
J Clin Invest. 2025 Mar 18;135(9). doi: 10.1172/JCI179572. eCollection 2025 May 1.
4
Vimentin modulates regulatory T cell receptor-ligand interactions at distal pole complex, leading to dysregulated host response to viral pneumonia.波形蛋白调节远极复合物处的调节性T细胞受体-配体相互作用,导致宿主对病毒性肺炎的反应失调。
Cell Rep. 2024 Dec 24;43(12):115056. doi: 10.1016/j.celrep.2024.115056. Epub 2024 Dec 7.
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