IL-22-producing RORγt-dependent innate lymphoid cells play a novel protective role in murine acute hepatitis.

Retinoid-related orphan receptor (ROR) γt is known to be related to the development and function of various immunological compartments in the liver, such as Th17 cells, natural killer T (NKT) cells, and innate lymphoid cells (ILCs). We evaluated the roles of RORγt-expressing cells in mouse acute hep...

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Autores principales:	Atsuhiro Matsumoto, Takanori Kanai, Yohei Mikami, Po-Sung Chu, Nobuhiro Nakamoto, Hirotoshi Ebinuma, Hidetsugu Saito, Toshiro Sato, Hideo Yagita, Toshifumi Hibi
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c9bf34da6ff1403ca39fda7316d88488
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spelling	oai:doaj.org-article:c9bf34da6ff1403ca39fda7316d884882021-11-18T07:48:12ZIL-22-producing RORγt-dependent innate lymphoid cells play a novel protective role in murine acute hepatitis.1932-620310.1371/journal.pone.0062853https://doaj.org/article/c9bf34da6ff1403ca39fda7316d884882013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23626860/?tool=EBIhttps://doaj.org/toc/1932-6203Retinoid-related orphan receptor (ROR) γt is known to be related to the development and function of various immunological compartments in the liver, such as Th17 cells, natural killer T (NKT) cells, and innate lymphoid cells (ILCs). We evaluated the roles of RORγt-expressing cells in mouse acute hepatitis model using RORγt deficient (RORγt(-/-)) mice and RAG-2 and RORγt double deficient (RAG-2(-/-) × RORγt(-/-)) mice. Acute hepatitis was induced in mice by injection with carbon tetrachloride (CCl4), to investigate the regulation of liver inflammation by RORγt-expressing cells. We detected RORC expression in three compartments, CD4(+) T cells, NKT cells, and lineage marker-negative SCA-1(+)Thy1(high) ILCs, of the liver of wild type (WT) mice. CCl4-treated RORγt(-/-) mice developed liver damage in spite of lack of RORγt-dependent cells, but with reduced infiltration of macrophages compared with WT mice. In this regard, ILCs were significantly decreased in RAG-2(-/-) × RORγt(-/-) mice that lacked T and NKT cells. Surprisingly, RAG-2(-/-) × RORγt(-/-) mice developed significantly severer CCl4-induced hepatitis compared with RAG-2(-/-) mice, in accordance with the fact that hepatic ILCs failed to produce IL-22. Lastly, anti-Thy1 monoclonal antibody (mAb), but not anti-NK1.1 mAb or anti-asialo GM1 Ab administration exacerbated liver damage in RAG-2(-/-) mice with the depletion of liver ILCs. Collectively, hepatic RORγt-dependent ILCs play a part of protective roles in hepatic immune response in mice.Atsuhiro MatsumotoTakanori KanaiYohei MikamiPo-Sung ChuNobuhiro NakamotoHirotoshi EbinumaHidetsugu SaitoToshiro SatoHideo YagitaToshifumi HibiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 4, p e62853 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Atsuhiro Matsumoto Takanori Kanai Yohei Mikami Po-Sung Chu Nobuhiro Nakamoto Hirotoshi Ebinuma Hidetsugu Saito Toshiro Sato Hideo Yagita Toshifumi Hibi IL-22-producing RORγt-dependent innate lymphoid cells play a novel protective role in murine acute hepatitis.
description	Retinoid-related orphan receptor (ROR) γt is known to be related to the development and function of various immunological compartments in the liver, such as Th17 cells, natural killer T (NKT) cells, and innate lymphoid cells (ILCs). We evaluated the roles of RORγt-expressing cells in mouse acute hepatitis model using RORγt deficient (RORγt(-/-)) mice and RAG-2 and RORγt double deficient (RAG-2(-/-) × RORγt(-/-)) mice. Acute hepatitis was induced in mice by injection with carbon tetrachloride (CCl4), to investigate the regulation of liver inflammation by RORγt-expressing cells. We detected RORC expression in three compartments, CD4(+) T cells, NKT cells, and lineage marker-negative SCA-1(+)Thy1(high) ILCs, of the liver of wild type (WT) mice. CCl4-treated RORγt(-/-) mice developed liver damage in spite of lack of RORγt-dependent cells, but with reduced infiltration of macrophages compared with WT mice. In this regard, ILCs were significantly decreased in RAG-2(-/-) × RORγt(-/-) mice that lacked T and NKT cells. Surprisingly, RAG-2(-/-) × RORγt(-/-) mice developed significantly severer CCl4-induced hepatitis compared with RAG-2(-/-) mice, in accordance with the fact that hepatic ILCs failed to produce IL-22. Lastly, anti-Thy1 monoclonal antibody (mAb), but not anti-NK1.1 mAb or anti-asialo GM1 Ab administration exacerbated liver damage in RAG-2(-/-) mice with the depletion of liver ILCs. Collectively, hepatic RORγt-dependent ILCs play a part of protective roles in hepatic immune response in mice.
format	article
author	Atsuhiro Matsumoto Takanori Kanai Yohei Mikami Po-Sung Chu Nobuhiro Nakamoto Hirotoshi Ebinuma Hidetsugu Saito Toshiro Sato Hideo Yagita Toshifumi Hibi
author_facet	Atsuhiro Matsumoto Takanori Kanai Yohei Mikami Po-Sung Chu Nobuhiro Nakamoto Hirotoshi Ebinuma Hidetsugu Saito Toshiro Sato Hideo Yagita Toshifumi Hibi
author_sort	Atsuhiro Matsumoto
title	IL-22-producing RORγt-dependent innate lymphoid cells play a novel protective role in murine acute hepatitis.
title_short	IL-22-producing RORγt-dependent innate lymphoid cells play a novel protective role in murine acute hepatitis.
title_full	IL-22-producing RORγt-dependent innate lymphoid cells play a novel protective role in murine acute hepatitis.
title_fullStr	IL-22-producing RORγt-dependent innate lymphoid cells play a novel protective role in murine acute hepatitis.
title_full_unstemmed	IL-22-producing RORγt-dependent innate lymphoid cells play a novel protective role in murine acute hepatitis.
title_sort	il-22-producing rorγt-dependent innate lymphoid cells play a novel protective role in murine acute hepatitis.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/c9bf34da6ff1403ca39fda7316d88488
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IL-22-producing RORγt-dependent innate lymphoid cells play a novel protective role in murine acute hepatitis.

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