NKG2A is a NK cell exhaustion checkpoint for HCV persistence

Immune cells may become less responsive, or ‘exhausted’, upon chronic viral infection, but the underlying mechanism and crosstalk are still unclear. Here the authors show that, upon chronic hepatitis C virus (HCV) infection, natural killer cell exhaustion is induced by NKG2A signalling to instruct d...

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Autores principales:	Chao Zhang, Xiao-mei Wang, Shu-ran Li, Trix Twelkmeyer, Wei-hong Wang, Sheng-yuan Zhang, Shu-feng Wang, Ji-zheng Chen, Xia Jin, Yu-zhang Wu, Xin-wen Chen, Sheng-dian Wang, Jun-qi Niu, Hai-rong Chen, Hong Tang
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2019
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/c0986ae00c854fd2a685f6ada664ab91
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spelling	oai:doaj.org-article:c0986ae00c854fd2a685f6ada664ab912021-12-02T16:58:05ZNKG2A is a NK cell exhaustion checkpoint for HCV persistence10.1038/s41467-019-09212-y2041-1723https://doaj.org/article/c0986ae00c854fd2a685f6ada664ab912019-04-01T00:00:00Zhttps://doi.org/10.1038/s41467-019-09212-yhttps://doaj.org/toc/2041-1723Immune cells may become less responsive, or ‘exhausted’, upon chronic viral infection, but the underlying mechanism and crosstalk are still unclear. Here the authors show that, upon chronic hepatitis C virus (HCV) infection, natural killer cell exhaustion is induced by NKG2A signalling to instruct downstream exhaustion of CD8+ T cells and HCV persistence.Chao ZhangXiao-mei WangShu-ran LiTrix TwelkmeyerWei-hong WangSheng-yuan ZhangShu-feng WangJi-zheng ChenXia JinYu-zhang WuXin-wen ChenSheng-dian WangJun-qi NiuHai-rong ChenHong TangNature PortfolioarticleScienceQENNature Communications, Vol 10, Iss 1, Pp 1-11 (2019)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Chao Zhang Xiao-mei Wang Shu-ran Li Trix Twelkmeyer Wei-hong Wang Sheng-yuan Zhang Shu-feng Wang Ji-zheng Chen Xia Jin Yu-zhang Wu Xin-wen Chen Sheng-dian Wang Jun-qi Niu Hai-rong Chen Hong Tang NKG2A is a NK cell exhaustion checkpoint for HCV persistence
description	Immune cells may become less responsive, or ‘exhausted’, upon chronic viral infection, but the underlying mechanism and crosstalk are still unclear. Here the authors show that, upon chronic hepatitis C virus (HCV) infection, natural killer cell exhaustion is induced by NKG2A signalling to instruct downstream exhaustion of CD8+ T cells and HCV persistence.
format	article
author	Chao Zhang Xiao-mei Wang Shu-ran Li Trix Twelkmeyer Wei-hong Wang Sheng-yuan Zhang Shu-feng Wang Ji-zheng Chen Xia Jin Yu-zhang Wu Xin-wen Chen Sheng-dian Wang Jun-qi Niu Hai-rong Chen Hong Tang
author_facet	Chao Zhang Xiao-mei Wang Shu-ran Li Trix Twelkmeyer Wei-hong Wang Sheng-yuan Zhang Shu-feng Wang Ji-zheng Chen Xia Jin Yu-zhang Wu Xin-wen Chen Sheng-dian Wang Jun-qi Niu Hai-rong Chen Hong Tang
author_sort	Chao Zhang
title	NKG2A is a NK cell exhaustion checkpoint for HCV persistence
title_short	NKG2A is a NK cell exhaustion checkpoint for HCV persistence
title_full	NKG2A is a NK cell exhaustion checkpoint for HCV persistence
title_fullStr	NKG2A is a NK cell exhaustion checkpoint for HCV persistence
title_full_unstemmed	NKG2A is a NK cell exhaustion checkpoint for HCV persistence
title_sort	nkg2a is a nk cell exhaustion checkpoint for hcv persistence
publisher	Nature Portfolio
publishDate	2019
url	https://doaj.org/article/c0986ae00c854fd2a685f6ada664ab91
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NKG2A is a NK cell exhaustion checkpoint for HCV persistence

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