Differential roles of regulatory T cells in acute respiratory infections

被引:12
|
作者
Jovisic, Milica [1 ,2 ]
Mambetsariev, Nurbek [3 ]
Singer, Benjamin D. [1 ,2 ,4 ,5 ]
Morales-Nebreda, Luisa [1 ,2 ,6 ]
机构
[1] Northwestern Univ, Dept Med, Div Pulm & Crit Care Med, Feinberg Sch Med, Chicago, IL USA
[2] Northwestern Univ, Simpson Querrey Lung Inst Translat Sci, Feinberg Sch Med, Chicago, IL USA
[3] Northwestern Univ, Dept Med, Div Allergy & Immunol, Feinberg Sch Med, Chicago, IL USA
[4] Northwestern Univ, Dept Biochem & Mol Genet, Feinberg Sch Med, Chicago, IL USA
[5] Northwestern Univ, Simpson Querrey Inst Epigenet, Feinberg Sch Med, Chicago, IL USA
[6] Simpson Querrey, 5th Floor, 303 E Super St, Chicago, IL 60611 USA
关键词
KERATINOCYTE GROWTH-FACTOR; SYNCYTIAL VIRUS-INFECTION; FOXP3; EXPRESSION; MEDIATOR COMPLEX; GUT MICROBIOTA; TISSUE-REPAIR; LUNG INJURY; TGF-BETA; INFLAMMATION; RESPONSES;
D O I
10.1172/JCI170505
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Acute respiratory infections trigger an inflammatory immune response with the goal of pathogen clearance; however, overexuberant inflammation causes tissue damage and impairs pulmonary function. CD4+FOXP3+ regulatory T cells (Tregs) interact with cells of both the innate and the adaptive immune system to limit acute pulmonary inflammation and promote its resolution. Tregs also provide tissue protection and coordinate lung tissue repair, facilitating a return to homeostatic pulmonary function. Here, we review Treg-mediated modulation of the host response to respiratory pathogens, focusing on mechanisms underlying how Tregs promote resolution of inflammation and repair of acute lung injury. We also discuss potential strategies to harness and optimize Tregs as a cellular therapy for patients with severe acute respiratory infection and discuss open questions in the field.
引用
收藏
页数:14
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