BTN2A2 protein negatively regulates T cells to ameliorate collagen-induced arthritis in mice

Abstract Rheumatoid arthritis (RA) is an autoimmune disorder characterized by persistent inflammatory responses in target tissues and organs, resulting in the destruction of joints. Collagen type II (CII)-induced arthritis (CIA) is the most used animal model for human RA. Although BTN2A2 protein has...

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Autores principales:	Xueping He, Rong Hu, Peng Luo, Jie Gao, Wenjiang Yang, Jiaju Li, Youjiao Huang, Feng Han, Laijun Lai, Min Su
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/02fc9199131d4e7797b1c8f23f939816
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spelling	oai:doaj.org-article:02fc9199131d4e7797b1c8f23f9398162021-12-02T17:37:35ZBTN2A2 protein negatively regulates T cells to ameliorate collagen-induced arthritis in mice10.1038/s41598-021-98443-52045-2322https://doaj.org/article/02fc9199131d4e7797b1c8f23f9398162021-09-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-98443-5https://doaj.org/toc/2045-2322Abstract Rheumatoid arthritis (RA) is an autoimmune disorder characterized by persistent inflammatory responses in target tissues and organs, resulting in the destruction of joints. Collagen type II (CII)-induced arthritis (CIA) is the most used animal model for human RA. Although BTN2A2 protein has been previously shown to inhibit T cell functions in vitro, its effect on autoimmune arthritis has not been reported. In this study, we investigate the ability of a recombinant BTN2A2-IgG2a Fc (BTN2A2-Ig) fusion protein to treat CIA. We show here that administration of BTN2A2-Ig attenuates established CIA, as compared with control Ig protein treatment. This is associated with reduced activation, proliferation and Th1/Th17 cytokine production of T cells in BTN2A2-Ig-treated CIA mice. BTN2A2-Ig also inhibits CII-specific T cell proliferation and Th1/Th17 cytokine production. Although the percentage of effector T cells is decreased in BTN2A2-Ig-treated CIA mice, the proportions of naive T cells and regulatory T cells is increased. Furthermore, BTN2A2-Ig reduces the percentage of proinflammatory M1 macrophages but increases the percentage of anti-inflammatory M2 macrophages in the CIA mice. Our results suggest that BTN2A2-Ig protein has the potential to be used in the treatment of collagen-induced arthritis models.Xueping HeRong HuPeng LuoJie GaoWenjiang YangJiaju LiYoujiao HuangFeng HanLaijun LaiMin SuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Xueping He Rong Hu Peng Luo Jie Gao Wenjiang Yang Jiaju Li Youjiao Huang Feng Han Laijun Lai Min Su BTN2A2 protein negatively regulates T cells to ameliorate collagen-induced arthritis in mice
description	Abstract Rheumatoid arthritis (RA) is an autoimmune disorder characterized by persistent inflammatory responses in target tissues and organs, resulting in the destruction of joints. Collagen type II (CII)-induced arthritis (CIA) is the most used animal model for human RA. Although BTN2A2 protein has been previously shown to inhibit T cell functions in vitro, its effect on autoimmune arthritis has not been reported. In this study, we investigate the ability of a recombinant BTN2A2-IgG2a Fc (BTN2A2-Ig) fusion protein to treat CIA. We show here that administration of BTN2A2-Ig attenuates established CIA, as compared with control Ig protein treatment. This is associated with reduced activation, proliferation and Th1/Th17 cytokine production of T cells in BTN2A2-Ig-treated CIA mice. BTN2A2-Ig also inhibits CII-specific T cell proliferation and Th1/Th17 cytokine production. Although the percentage of effector T cells is decreased in BTN2A2-Ig-treated CIA mice, the proportions of naive T cells and regulatory T cells is increased. Furthermore, BTN2A2-Ig reduces the percentage of proinflammatory M1 macrophages but increases the percentage of anti-inflammatory M2 macrophages in the CIA mice. Our results suggest that BTN2A2-Ig protein has the potential to be used in the treatment of collagen-induced arthritis models.
format	article
author	Xueping He Rong Hu Peng Luo Jie Gao Wenjiang Yang Jiaju Li Youjiao Huang Feng Han Laijun Lai Min Su
author_facet	Xueping He Rong Hu Peng Luo Jie Gao Wenjiang Yang Jiaju Li Youjiao Huang Feng Han Laijun Lai Min Su
author_sort	Xueping He
title	BTN2A2 protein negatively regulates T cells to ameliorate collagen-induced arthritis in mice
title_short	BTN2A2 protein negatively regulates T cells to ameliorate collagen-induced arthritis in mice
title_full	BTN2A2 protein negatively regulates T cells to ameliorate collagen-induced arthritis in mice
title_fullStr	BTN2A2 protein negatively regulates T cells to ameliorate collagen-induced arthritis in mice
title_full_unstemmed	BTN2A2 protein negatively regulates T cells to ameliorate collagen-induced arthritis in mice
title_sort	btn2a2 protein negatively regulates t cells to ameliorate collagen-induced arthritis in mice
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/02fc9199131d4e7797b1c8f23f939816
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BTN2A2 protein negatively regulates T cells to ameliorate collagen-induced arthritis in mice

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