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Title: An upregulation of CD8{sup +}CD25{sup +}Foxp3{sup +} T cells with suppressive function through interleukin 2 pathway in pulmonary arterial hypertension

Journal Article · · Experimental Cell Research

Accumulating evidence suggests that abnormal inflammation plays a critical role in the pathogenesis of pulmonary arterial hypertension (PAH). CD8{sup +}CD25{sup +}Foxp3{sup +} T cell is a novel cell subtype, and its role in PAH is not yet investigated. Here, we observed that PAH patients presented a significant upregulation of CD8{sup +}CD25{sup +}Foxp3{sup +} T cells and a downregulation of CD4{sup +}CD25{sup +}Foxp3{sup +} T cells compared to healthy controls. Regardless, the total number of CD25{sup +}Foxp3{sup +} T cells in PAH patients was still smaller than that in healthy controls. Compared to CD8{sup +}CD25{sup -} T cells, CD8{sup +}CD25{sup +} T cells presented higher Foxp3 expression, lower interferon (IFN)-γ expression and higher transforming growth factor (TGF)-β expression, in both healthy and PAH individuals. The CD8{sup +}CD25{sup +} T cells in PAH patients also demonstrated regulatory function by suppressing the proliferation of CD4{sup +}CD25{sup -} and CD8{sup +}CD25{sup -} effector T cells, albeit at lower efficiency than CD4{sup +}CD25{sup +} T cells from PAH patients and healthy volunteers. CD8{sup +}CD25{sup +} T cells from PAH responded to interleukin (IL)−2 supplement by expansion and upregulating Foxp3 expression. In PAH patients, IL-2-treated CD8{sup +}CD25{sup +} T cells were more potent at inhibiting CD4{sup +}CD25{sup -} effector T cell proliferation than IL-2-untreated CD8{sup +}CD25{sup +} T cells. Together, we found an upregulation of CD8{sup +}CD25{sup +}Foxp3{sup +} T cells in PAH patients, and this T cell population presented suppressive activity that could be enhanced by IL-2 treatment.

OSTI ID:
22738154
Journal Information:
Experimental Cell Research, Vol. 358, Issue 2; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
Country of Publication:
United States
Language:
English