The Role of Regulatory T Cells in Pulmonary Arterial Hypertension

被引：35

作者：

Tian, Wen ^{[1
,2
]}

Jiang, Shirley Y. ^{[2
]}

Jiang, Xinguo ^{[1
,2
]}

Tamosiuniene, Rasa ^{[1
]}

Kim, Dongeon ^{[2
]}

Guan, Torrey ^{[1
]}

Arsalane, Siham ^{[1
,2
]}

Pasupneti, Shravani ^{[2
]}

Voelkel, Norbert F. ^{[3
]}

Tang, Qizhi ^{[4
]}

Nicolls, Mark R. ^{[1
,2
]}

机构：

[1] VA Palo Alto Hlth Care Syst, Dept Med, Palo Alto, CA 94304 USA

[2] Stanford Univ, Sch Med, Dept Med, Stanford, CA 94305 USA

[3] Univ Amsterdam, Med Ctr, Dept Pulm Med, Amsterdam, Netherlands

[4] Univ Calif San Francisco, Dept Surg, San Francisco, CA USA

来源：

FRONTIERS IN IMMUNOLOGY | 2021年 / 12卷

基金：

美国国家卫生研究院;

关键词：

regulatory T cell; pulmonary arterial hypertension; sexual dimorphism; right ventricle; estrogen; SEX-DIFFERENCES; FOXP3; EXPRESSION; ESTROGEN; IMMUNE; TREG; HUMAN-HERPESVIRUS-8; PATHOBIOLOGY; AUTOIMMUNITY; PATHOGENESIS; KYNURENINE;

D O I：

10.3389/fimmu.2021.684657

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Pulmonary arterial hypertension (PAH) is a chronic, incurable condition characterized by pulmonary vascular remodeling, perivascular inflammation, and right heart failure. Regulatory T cells (Tregs) stave off autoimmunity, and there is increasing evidence for their compromised activity in the inflammatory milieu of PAH. Abnormal Treg function is strongly correlated with a predisposition to PAH in animals and patients. Athymic Treg-depleted rats treated with SU5416, an agent causing pulmonary vascular injury, develop PAH, which is prevented by infusing missing CD4(+)CD25(high)FOXP3(+) Tregs. Abnormal Treg activity may also explain why PAH disproportionately affects women more than men. This mini review focuses on the role of Tregs in PAH with a special view to sexual dimorphism and the future promise of Treg therapy.

引用

页数：9

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