Programmed death one homolog maintains the pool size of regulatory T cells by promoting their differentiation and stability

Abstract Programmed death one homolog (PD-1H) is an immunoglobulin superfamily molecule and primarily acts as a coinhibitor in the initiation of T cell response to antigens. Here, we report that genetic ablation of PD-1H in mice blocks the differentiation of naive T cells to Foxp3+ inducible Treg ce...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Qi Wang, Jianwei He, Dallas B. Flies, Liqun Luo, Lieping Chen
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/1bf05031662a44279ebcf81319210322
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:1bf05031662a44279ebcf81319210322
record_format	dspace
spelling	oai:doaj.org-article:1bf05031662a44279ebcf813192103222021-12-02T15:06:10ZProgrammed death one homolog maintains the pool size of regulatory T cells by promoting their differentiation and stability10.1038/s41598-017-06410-w2045-2322https://doaj.org/article/1bf05031662a44279ebcf813192103222017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06410-whttps://doaj.org/toc/2045-2322Abstract Programmed death one homolog (PD-1H) is an immunoglobulin superfamily molecule and primarily acts as a coinhibitor in the initiation of T cell response to antigens. Here, we report that genetic ablation of PD-1H in mice blocks the differentiation of naive T cells to Foxp3+ inducible Treg cells (iTreg) with a significant decrease of iTreg in lymphoid organs. This effect of PD-1H is highly specific for iTreg because both naturally generated iTreg in gut-related tissues and in vitro induced iTreg by TGF-β were decreased whereas the genesis of natural Treg (nTreg) remains normal. The suppressive function of both iTreg and nTreg, however, is not affected by the loss of PD-1H. In addition to decreased production, PD-1H deficient iTreg could also rapidly convert to CD4+ T helper 1 or T helper 17 cells in an inflammatory environment. Our results indicate that PD-1H is required for maintenance of iTreg pool size by promoting its differentiation and preventing its conversion to other CD4+ T cell subsets. These findings may have important implications for manipulating Tregs to control inflammation.Qi WangJianwei HeDallas B. FliesLiqun LuoLieping ChenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Qi Wang Jianwei He Dallas B. Flies Liqun Luo Lieping Chen Programmed death one homolog maintains the pool size of regulatory T cells by promoting their differentiation and stability
description	Abstract Programmed death one homolog (PD-1H) is an immunoglobulin superfamily molecule and primarily acts as a coinhibitor in the initiation of T cell response to antigens. Here, we report that genetic ablation of PD-1H in mice blocks the differentiation of naive T cells to Foxp3+ inducible Treg cells (iTreg) with a significant decrease of iTreg in lymphoid organs. This effect of PD-1H is highly specific for iTreg because both naturally generated iTreg in gut-related tissues and in vitro induced iTreg by TGF-β were decreased whereas the genesis of natural Treg (nTreg) remains normal. The suppressive function of both iTreg and nTreg, however, is not affected by the loss of PD-1H. In addition to decreased production, PD-1H deficient iTreg could also rapidly convert to CD4+ T helper 1 or T helper 17 cells in an inflammatory environment. Our results indicate that PD-1H is required for maintenance of iTreg pool size by promoting its differentiation and preventing its conversion to other CD4+ T cell subsets. These findings may have important implications for manipulating Tregs to control inflammation.
format	article
author	Qi Wang Jianwei He Dallas B. Flies Liqun Luo Lieping Chen
author_facet	Qi Wang Jianwei He Dallas B. Flies Liqun Luo Lieping Chen
author_sort	Qi Wang
title	Programmed death one homolog maintains the pool size of regulatory T cells by promoting their differentiation and stability
title_short	Programmed death one homolog maintains the pool size of regulatory T cells by promoting their differentiation and stability
title_full	Programmed death one homolog maintains the pool size of regulatory T cells by promoting their differentiation and stability
title_fullStr	Programmed death one homolog maintains the pool size of regulatory T cells by promoting their differentiation and stability
title_full_unstemmed	Programmed death one homolog maintains the pool size of regulatory T cells by promoting their differentiation and stability
title_sort	programmed death one homolog maintains the pool size of regulatory t cells by promoting their differentiation and stability
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/1bf05031662a44279ebcf81319210322
work_keys_str_mv	AT qiwang programmeddeathonehomologmaintainsthepoolsizeofregulatorytcellsbypromotingtheirdifferentiationandstability AT jianweihe programmeddeathonehomologmaintainsthepoolsizeofregulatorytcellsbypromotingtheirdifferentiationandstability AT dallasbflies programmeddeathonehomologmaintainsthepoolsizeofregulatorytcellsbypromotingtheirdifferentiationandstability AT liqunluo programmeddeathonehomologmaintainsthepoolsizeofregulatorytcellsbypromotingtheirdifferentiationandstability AT liepingchen programmeddeathonehomologmaintainsthepoolsizeofregulatorytcellsbypromotingtheirdifferentiationandstability
_version_	1718388564386906112

Programmed death one homolog maintains the pool size of regulatory T cells by promoting their differentiation and stability

Ejemplares similares