IL-17A reprograms intestinal epithelial cells to facilitate HIV-1 replication and outgrowth in CD4+ T cells

Summary: The crosstalk between intestinal epithelial cells (IECs) and Th17-polarized CD4+ T cells is critical for mucosal homeostasis, with HIV-1 causing significant alterations in people living with HIV (PLWH) despite antiretroviral therapy (ART). In a model of IEC and T cell co-cultures, we invest...

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Autores principales:	Tomas Raul Wiche Salinas, Annie Gosselin, Laurence Raymond Marchand, Etiene Moreira Gabriel, Olivier Tastet, Jean-Philippe Goulet, Yuwei Zhang, Dragos Vlad, Hanane Touil, Jean-Pierre Routy, Mariana G. Bego, Mohamed El-Far, Nicolas Chomont, Alan L. Landay, Éric A. Cohen, Cécile Tremblay, Petronela Ancuta
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	Immunology Immune response Virology Science Q
Acceso en línea:	https://doaj.org/article/11fcfb2c9afd4ce1af686fd523cb4e06
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spelling	oai:doaj.org-article:11fcfb2c9afd4ce1af686fd523cb4e062021-11-20T05:08:29ZIL-17A reprograms intestinal epithelial cells to facilitate HIV-1 replication and outgrowth in CD4+ T cells2589-004210.1016/j.isci.2021.103225https://doaj.org/article/11fcfb2c9afd4ce1af686fd523cb4e062021-11-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2589004221011937https://doaj.org/toc/2589-0042Summary: The crosstalk between intestinal epithelial cells (IECs) and Th17-polarized CD4+ T cells is critical for mucosal homeostasis, with HIV-1 causing significant alterations in people living with HIV (PLWH) despite antiretroviral therapy (ART). In a model of IEC and T cell co-cultures, we investigated the effects of IL-17A, the Th17 hallmark cytokine, on IEC ability to promote de novo HIV infection and viral reservoir reactivation. Our results demonstrate that IL-17A acts in synergy with TNF to boost IEC production of CCL20, a Th17-attractant chemokine, and promote HIV trans-infection of CD4+ T cells and viral outgrowth from reservoir cells of ART-treated PLWH. Importantly, the Illumina RNA-sequencing revealed an IL-17A-mediated pro-inflammatory and pro-viral molecular signature, including a decreased expression of type I interferon (IFN-I)-induced HIV restriction factors. These findings point to the deleterious features of IL-17A and raise awareness for caution when designing therapies aimed at restoring the paucity of mucosal Th17 cells in ART-treated PLWH.Tomas Raul Wiche SalinasAnnie GosselinLaurence Raymond MarchandEtiene Moreira GabrielOlivier TastetJean-Philippe GouletYuwei ZhangDragos VladHanane TouilJean-Pierre RoutyMariana G. BegoMohamed El-FarNicolas ChomontAlan L. LandayÉric A. CohenCécile TremblayPetronela AncutaElsevierarticleImmunologyImmune responseVirologyScienceQENiScience, Vol 24, Iss 11, Pp 103225- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunology Immune response Virology Science Q
spellingShingle	Immunology Immune response Virology Science Q Tomas Raul Wiche Salinas Annie Gosselin Laurence Raymond Marchand Etiene Moreira Gabriel Olivier Tastet Jean-Philippe Goulet Yuwei Zhang Dragos Vlad Hanane Touil Jean-Pierre Routy Mariana G. Bego Mohamed El-Far Nicolas Chomont Alan L. Landay Éric A. Cohen Cécile Tremblay Petronela Ancuta IL-17A reprograms intestinal epithelial cells to facilitate HIV-1 replication and outgrowth in CD4+ T cells
description	Summary: The crosstalk between intestinal epithelial cells (IECs) and Th17-polarized CD4+ T cells is critical for mucosal homeostasis, with HIV-1 causing significant alterations in people living with HIV (PLWH) despite antiretroviral therapy (ART). In a model of IEC and T cell co-cultures, we investigated the effects of IL-17A, the Th17 hallmark cytokine, on IEC ability to promote de novo HIV infection and viral reservoir reactivation. Our results demonstrate that IL-17A acts in synergy with TNF to boost IEC production of CCL20, a Th17-attractant chemokine, and promote HIV trans-infection of CD4+ T cells and viral outgrowth from reservoir cells of ART-treated PLWH. Importantly, the Illumina RNA-sequencing revealed an IL-17A-mediated pro-inflammatory and pro-viral molecular signature, including a decreased expression of type I interferon (IFN-I)-induced HIV restriction factors. These findings point to the deleterious features of IL-17A and raise awareness for caution when designing therapies aimed at restoring the paucity of mucosal Th17 cells in ART-treated PLWH.
format	article
author	Tomas Raul Wiche Salinas Annie Gosselin Laurence Raymond Marchand Etiene Moreira Gabriel Olivier Tastet Jean-Philippe Goulet Yuwei Zhang Dragos Vlad Hanane Touil Jean-Pierre Routy Mariana G. Bego Mohamed El-Far Nicolas Chomont Alan L. Landay Éric A. Cohen Cécile Tremblay Petronela Ancuta
author_facet	Tomas Raul Wiche Salinas Annie Gosselin Laurence Raymond Marchand Etiene Moreira Gabriel Olivier Tastet Jean-Philippe Goulet Yuwei Zhang Dragos Vlad Hanane Touil Jean-Pierre Routy Mariana G. Bego Mohamed El-Far Nicolas Chomont Alan L. Landay Éric A. Cohen Cécile Tremblay Petronela Ancuta
author_sort	Tomas Raul Wiche Salinas
title	IL-17A reprograms intestinal epithelial cells to facilitate HIV-1 replication and outgrowth in CD4+ T cells
title_short	IL-17A reprograms intestinal epithelial cells to facilitate HIV-1 replication and outgrowth in CD4+ T cells
title_full	IL-17A reprograms intestinal epithelial cells to facilitate HIV-1 replication and outgrowth in CD4+ T cells
title_fullStr	IL-17A reprograms intestinal epithelial cells to facilitate HIV-1 replication and outgrowth in CD4+ T cells
title_full_unstemmed	IL-17A reprograms intestinal epithelial cells to facilitate HIV-1 replication and outgrowth in CD4+ T cells
title_sort	il-17a reprograms intestinal epithelial cells to facilitate hiv-1 replication and outgrowth in cd4+ t cells
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/11fcfb2c9afd4ce1af686fd523cb4e06
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IL-17A reprograms intestinal epithelial cells to facilitate HIV-1 replication and outgrowth in CD4+ T cells

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