NKG2D modulates aggravation of liver inflammation by activating NK cells in HBV infection

Abstract Hepatitis B virus (HBV) infection is thought to be an immune-mediated liver disease. The mechanisms underlying natural killer (NK) cell group 2D receptor (NKG2D) that activates NK cells and participates in anti-HBV immunity and immunopathology has not been thoroughly elucidated. Peripheral...

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Autores principales:	Yadong Wang, Wei Wang, Chuan Shen, Yong Wang, Mingjing Jiao, Weiyan Yu, Hongzhu Yin, Xiaobo Shang, Qianfei Liang, Caiyan Zhao
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/67567fb11a5c4b1aa5073ea5185c3bdc
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spelling	oai:doaj.org-article:67567fb11a5c4b1aa5073ea5185c3bdc2021-12-02T16:08:22ZNKG2D modulates aggravation of liver inflammation by activating NK cells in HBV infection10.1038/s41598-017-00221-92045-2322https://doaj.org/article/67567fb11a5c4b1aa5073ea5185c3bdc2017-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-00221-9https://doaj.org/toc/2045-2322Abstract Hepatitis B virus (HBV) infection is thought to be an immune-mediated liver disease. The mechanisms underlying natural killer (NK) cell group 2D receptor (NKG2D) that activates NK cells and participates in anti-HBV immunity and immunopathology has not been thoroughly elucidated. Peripheral NKG2D+ and IFN-γ+ NK cells frequencies and intrahepatic NKG2D and IFN-γ mRNA and protein expressions were determined in HBV-infected patients. Levels of NKG2D and IFN-γ mRNA and protein in NK cells, co-cultured with HBV-replicating HepG2 cells with or without NKG2D blockade, were analyzed. Serum and supernatant IFN-γ, TNF-α, perforin and granzyme B were measured. In results, peripheral NKG2D+ and IFN-γ+ NK cells frequencies, intrahepatic NKG2D and IFN-γ mRNA and protein levels, and serum IFN-γ, TNF-α, perforin and granzyme B levels were all highest in HBV-related acute-on-chronic liver failure group, followed by chronic hepatitis B and chronic HBV carrier groups. In vitro, NKG2D and IFN-γ mRNA and protein levels were higher in NK cells with IFN-α stimulation than without stimulation. Supernatant IFN-γ, TNF-α, perforin and granzyme B levels were increased under co-culture or IFN-α stimulating conditions, but were partially blocked by NKG2DmAb. In conclusion, NKG2D regulates immune inflammation and anti-viral response partly through activation of NK cells during HBV infection.Yadong WangWei WangChuan ShenYong WangMingjing JiaoWeiyan YuHongzhu YinXiaobo ShangQianfei LiangCaiyan ZhaoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yadong Wang Wei Wang Chuan Shen Yong Wang Mingjing Jiao Weiyan Yu Hongzhu Yin Xiaobo Shang Qianfei Liang Caiyan Zhao NKG2D modulates aggravation of liver inflammation by activating NK cells in HBV infection
description	Abstract Hepatitis B virus (HBV) infection is thought to be an immune-mediated liver disease. The mechanisms underlying natural killer (NK) cell group 2D receptor (NKG2D) that activates NK cells and participates in anti-HBV immunity and immunopathology has not been thoroughly elucidated. Peripheral NKG2D+ and IFN-γ+ NK cells frequencies and intrahepatic NKG2D and IFN-γ mRNA and protein expressions were determined in HBV-infected patients. Levels of NKG2D and IFN-γ mRNA and protein in NK cells, co-cultured with HBV-replicating HepG2 cells with or without NKG2D blockade, were analyzed. Serum and supernatant IFN-γ, TNF-α, perforin and granzyme B were measured. In results, peripheral NKG2D+ and IFN-γ+ NK cells frequencies, intrahepatic NKG2D and IFN-γ mRNA and protein levels, and serum IFN-γ, TNF-α, perforin and granzyme B levels were all highest in HBV-related acute-on-chronic liver failure group, followed by chronic hepatitis B and chronic HBV carrier groups. In vitro, NKG2D and IFN-γ mRNA and protein levels were higher in NK cells with IFN-α stimulation than without stimulation. Supernatant IFN-γ, TNF-α, perforin and granzyme B levels were increased under co-culture or IFN-α stimulating conditions, but were partially blocked by NKG2DmAb. In conclusion, NKG2D regulates immune inflammation and anti-viral response partly through activation of NK cells during HBV infection.
format	article
author	Yadong Wang Wei Wang Chuan Shen Yong Wang Mingjing Jiao Weiyan Yu Hongzhu Yin Xiaobo Shang Qianfei Liang Caiyan Zhao
author_facet	Yadong Wang Wei Wang Chuan Shen Yong Wang Mingjing Jiao Weiyan Yu Hongzhu Yin Xiaobo Shang Qianfei Liang Caiyan Zhao
author_sort	Yadong Wang
title	NKG2D modulates aggravation of liver inflammation by activating NK cells in HBV infection
title_short	NKG2D modulates aggravation of liver inflammation by activating NK cells in HBV infection
title_full	NKG2D modulates aggravation of liver inflammation by activating NK cells in HBV infection
title_fullStr	NKG2D modulates aggravation of liver inflammation by activating NK cells in HBV infection
title_full_unstemmed	NKG2D modulates aggravation of liver inflammation by activating NK cells in HBV infection
title_sort	nkg2d modulates aggravation of liver inflammation by activating nk cells in hbv infection
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/67567fb11a5c4b1aa5073ea5185c3bdc
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NKG2D modulates aggravation of liver inflammation by activating NK cells in HBV infection

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