A tightly regulated IL-22 response maintains immune functions and homeostasis in systemic viral infection

Abstract Interleukin-22 (IL-22) plays an important role in host immunity and tissue homeostasis in infectious and inflammatory diseases. However, the function and regulation of IL-22 in viral infection remain largely unknown. Here, we report that viral infection triggered early IL-22 production from...

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Autores principales:	Panpan Yi, Yuejin Liang, Denley Ming Kee Yuan, Zuliang Jie, Zakari Kwota, Yan Chen, Yingzi Cong, Xuegong Fan, Jiaren Sun
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/73e6efb19bd94669bb547c8562695500
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spelling	oai:doaj.org-article:73e6efb19bd94669bb547c85626955002021-12-02T11:40:21ZA tightly regulated IL-22 response maintains immune functions and homeostasis in systemic viral infection10.1038/s41598-017-04260-02045-2322https://doaj.org/article/73e6efb19bd94669bb547c85626955002017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-04260-0https://doaj.org/toc/2045-2322Abstract Interleukin-22 (IL-22) plays an important role in host immunity and tissue homeostasis in infectious and inflammatory diseases. However, the function and regulation of IL-22 in viral infection remain largely unknown. Here, we report that viral infection triggered early IL-22 production from the liver and lymphoid organs. γδ T cells are the main immune cells to produce IL-22 in the liver, a process mediated by the IL-23/phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin complex 1 (mTORC1) signaling pathway. In the presence of IL-23, IL-22 production is independent of aryl hydrocarbon receptor (AhR) signaling. In acute and persistent viral infections, IL-22 deficiency resulted in thymic and splenic hypertrophy, while excessive IL-22 induced atrophy in these lymphoid organs. Moreover, IL-22 deficiency enhanced T cell responses to promote viral clearance, but increased IL-22 in vivo decreased T cell numbers and functions in the liver and lymphoid tissues. Together, our findings reveal a significant effect of the IL-23/PI3K/mTORC1 axis on regulating IL-22 production and also identify a novel role of IL-22 in controlling antiviral T cell responses in the non-lymphoid and lymphoid organs during acute and persistent viral infections.Panpan YiYuejin LiangDenley Ming Kee YuanZuliang JieZakari KwotaYan ChenYingzi CongXuegong FanJiaren SunNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Panpan Yi Yuejin Liang Denley Ming Kee Yuan Zuliang Jie Zakari Kwota Yan Chen Yingzi Cong Xuegong Fan Jiaren Sun A tightly regulated IL-22 response maintains immune functions and homeostasis in systemic viral infection
description	Abstract Interleukin-22 (IL-22) plays an important role in host immunity and tissue homeostasis in infectious and inflammatory diseases. However, the function and regulation of IL-22 in viral infection remain largely unknown. Here, we report that viral infection triggered early IL-22 production from the liver and lymphoid organs. γδ T cells are the main immune cells to produce IL-22 in the liver, a process mediated by the IL-23/phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin complex 1 (mTORC1) signaling pathway. In the presence of IL-23, IL-22 production is independent of aryl hydrocarbon receptor (AhR) signaling. In acute and persistent viral infections, IL-22 deficiency resulted in thymic and splenic hypertrophy, while excessive IL-22 induced atrophy in these lymphoid organs. Moreover, IL-22 deficiency enhanced T cell responses to promote viral clearance, but increased IL-22 in vivo decreased T cell numbers and functions in the liver and lymphoid tissues. Together, our findings reveal a significant effect of the IL-23/PI3K/mTORC1 axis on regulating IL-22 production and also identify a novel role of IL-22 in controlling antiviral T cell responses in the non-lymphoid and lymphoid organs during acute and persistent viral infections.
format	article
author	Panpan Yi Yuejin Liang Denley Ming Kee Yuan Zuliang Jie Zakari Kwota Yan Chen Yingzi Cong Xuegong Fan Jiaren Sun
author_facet	Panpan Yi Yuejin Liang Denley Ming Kee Yuan Zuliang Jie Zakari Kwota Yan Chen Yingzi Cong Xuegong Fan Jiaren Sun
author_sort	Panpan Yi
title	A tightly regulated IL-22 response maintains immune functions and homeostasis in systemic viral infection
title_short	A tightly regulated IL-22 response maintains immune functions and homeostasis in systemic viral infection
title_full	A tightly regulated IL-22 response maintains immune functions and homeostasis in systemic viral infection
title_fullStr	A tightly regulated IL-22 response maintains immune functions and homeostasis in systemic viral infection
title_full_unstemmed	A tightly regulated IL-22 response maintains immune functions and homeostasis in systemic viral infection
title_sort	tightly regulated il-22 response maintains immune functions and homeostasis in systemic viral infection
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/73e6efb19bd94669bb547c8562695500
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A tightly regulated IL-22 response maintains immune functions and homeostasis in systemic viral infection

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