CXCR6+CD4+ T cells promote mortality during Trypanosoma brucei infection.

Liver macrophages internalize circulating bloodborne parasites. It remains poorly understood how this process affects the fate of the macrophages and T cell responses in the liver. Here, we report that infection by Trypanosoma brucei induced depletion of macrophages in the liver, leading to the repo...

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Autores principales:	Gongguan Liu, Osama Abas, Ashley B Strickland, Yanli Chen, Meiqing Shi
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/956367ea935c47b5947d253a57a7745d
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spelling	oai:doaj.org-article:956367ea935c47b5947d253a57a7745d2021-12-02T20:00:04ZCXCR6+CD4+ T cells promote mortality during Trypanosoma brucei infection.1553-73661553-737410.1371/journal.ppat.1009968https://doaj.org/article/956367ea935c47b5947d253a57a7745d2021-10-01T00:00:00Zhttps://doi.org/10.1371/journal.ppat.1009968https://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Liver macrophages internalize circulating bloodborne parasites. It remains poorly understood how this process affects the fate of the macrophages and T cell responses in the liver. Here, we report that infection by Trypanosoma brucei induced depletion of macrophages in the liver, leading to the repopulation of CXCL16-secreting intrahepatic macrophages, associated with substantial accumulation of CXCR6+CD4+ T cells in the liver. Interestingly, disruption of CXCR6 signaling did not affect control of the parasitemia, but significantly enhanced the survival of infected mice, associated with reduced inflammation and liver injury. Infected CXCR6 deficient mice displayed a reduced accumulation of CD4+ T cells in the liver; adoptive transfer experiments suggested that the reduction of CD4+ T cells in the liver was attributed to a cell intrinsic property of CXCR6 deficient CD4+ T cells. Importantly, infected CXCR6 deficient mice receiving wild-type CD4+ T cells survived significantly shorter than those receiving CXCR6 deficient CD4+ T cells, demonstrating that CXCR6+CD4+ T cells promote the mortality. We conclude that infection of T. brucei leads to depletion and repopulation of liver macrophages, associated with a substantial influx of CXCR6+CD4+ T cells that mediates mortality.Gongguan LiuOsama AbasAshley B StricklandYanli ChenMeiqing ShiPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 17, Iss 10, p e1009968 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Gongguan Liu Osama Abas Ashley B Strickland Yanli Chen Meiqing Shi CXCR6+CD4+ T cells promote mortality during Trypanosoma brucei infection.
description	Liver macrophages internalize circulating bloodborne parasites. It remains poorly understood how this process affects the fate of the macrophages and T cell responses in the liver. Here, we report that infection by Trypanosoma brucei induced depletion of macrophages in the liver, leading to the repopulation of CXCL16-secreting intrahepatic macrophages, associated with substantial accumulation of CXCR6+CD4+ T cells in the liver. Interestingly, disruption of CXCR6 signaling did not affect control of the parasitemia, but significantly enhanced the survival of infected mice, associated with reduced inflammation and liver injury. Infected CXCR6 deficient mice displayed a reduced accumulation of CD4+ T cells in the liver; adoptive transfer experiments suggested that the reduction of CD4+ T cells in the liver was attributed to a cell intrinsic property of CXCR6 deficient CD4+ T cells. Importantly, infected CXCR6 deficient mice receiving wild-type CD4+ T cells survived significantly shorter than those receiving CXCR6 deficient CD4+ T cells, demonstrating that CXCR6+CD4+ T cells promote the mortality. We conclude that infection of T. brucei leads to depletion and repopulation of liver macrophages, associated with a substantial influx of CXCR6+CD4+ T cells that mediates mortality.
format	article
author	Gongguan Liu Osama Abas Ashley B Strickland Yanli Chen Meiqing Shi
author_facet	Gongguan Liu Osama Abas Ashley B Strickland Yanli Chen Meiqing Shi
author_sort	Gongguan Liu
title	CXCR6+CD4+ T cells promote mortality during Trypanosoma brucei infection.
title_short	CXCR6+CD4+ T cells promote mortality during Trypanosoma brucei infection.
title_full	CXCR6+CD4+ T cells promote mortality during Trypanosoma brucei infection.
title_fullStr	CXCR6+CD4+ T cells promote mortality during Trypanosoma brucei infection.
title_full_unstemmed	CXCR6+CD4+ T cells promote mortality during Trypanosoma brucei infection.
title_sort	cxcr6+cd4+ t cells promote mortality during trypanosoma brucei infection.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/956367ea935c47b5947d253a57a7745d
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CXCR6+CD4+ T cells promote mortality during Trypanosoma brucei infection.

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