Myeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection

There are several mechanisms by which human immunodeficiency virus (HIV) can mediate immune dysfunction and exhaustion during the course of infection. Chronic immune activation, after HIV infection, seems to be a key driving force of such unwanted consequences, which in turn worsens the pathological...

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Autores principales:	Mahmoud Mohammad Yaseen, Nizar Mohammad Abuharfeil, Homa Darmani
Formato:	article
Lenguaje:	EN
Publicado:	The Royal Society 2021
Materias:	tat protein gp120 PD-1/PD-l1 regulatory T (treg) cells microbial translocation T-cell dysfunction Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/15c9867111ec4027b417fa6f0c846901
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spelling	oai:doaj.org-article:15c9867111ec4027b417fa6f0c8469012021-11-10T08:06:38ZMyeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection10.1098/rsob.2102162046-2441https://doaj.org/article/15c9867111ec4027b417fa6f0c8469012021-11-01T00:00:00Zhttps://royalsocietypublishing.org/doi/10.1098/rsob.210216https://doaj.org/toc/2046-2441There are several mechanisms by which human immunodeficiency virus (HIV) can mediate immune dysfunction and exhaustion during the course of infection. Chronic immune activation, after HIV infection, seems to be a key driving force of such unwanted consequences, which in turn worsens the pathological status. In such cases, the immune system is programmed to initiate responses that counteract unwanted immune activation, for example through the expansion of myeloid-derived suppressor cells (MDSCs). Although the expansion of immune suppressor cells in the setting of systemic chronic immune activation, in theory, is expected to contain immune activation, HIV infection is still associated with a remarkably high level of biomarkers of immune activation. Paradoxically, the expansion of immune suppressor cells during HIV infection can suppress potent anti-viral immune responses, which in turn contribute to viral persistence and disease progression. This indicates that HIV hijacks not only immune activation but also the immune regulatory responses to its advantage. In this work, we aim to pave the way to comprehend how such unwanted expansion of MDSCs could participate in the pathology of acute/primary and chronic HIV infection in humans, as well as simian immunodeficiency virus infection in rhesus macaques, according to the available literature.Mahmoud Mohammad YaseenNizar Mohammad AbuharfeilHoma DarmaniThe Royal Societyarticletat proteingp120PD-1/PD-l1regulatory T (treg) cellsmicrobial translocationT-cell dysfunctionBiology (General)QH301-705.5ENOpen Biology, Vol 11, Iss 11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	tat protein gp120 PD-1/PD-l1 regulatory T (treg) cells microbial translocation T-cell dysfunction Biology (General) QH301-705.5
spellingShingle	tat protein gp120 PD-1/PD-l1 regulatory T (treg) cells microbial translocation T-cell dysfunction Biology (General) QH301-705.5 Mahmoud Mohammad Yaseen Nizar Mohammad Abuharfeil Homa Darmani Myeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection
description	There are several mechanisms by which human immunodeficiency virus (HIV) can mediate immune dysfunction and exhaustion during the course of infection. Chronic immune activation, after HIV infection, seems to be a key driving force of such unwanted consequences, which in turn worsens the pathological status. In such cases, the immune system is programmed to initiate responses that counteract unwanted immune activation, for example through the expansion of myeloid-derived suppressor cells (MDSCs). Although the expansion of immune suppressor cells in the setting of systemic chronic immune activation, in theory, is expected to contain immune activation, HIV infection is still associated with a remarkably high level of biomarkers of immune activation. Paradoxically, the expansion of immune suppressor cells during HIV infection can suppress potent anti-viral immune responses, which in turn contribute to viral persistence and disease progression. This indicates that HIV hijacks not only immune activation but also the immune regulatory responses to its advantage. In this work, we aim to pave the way to comprehend how such unwanted expansion of MDSCs could participate in the pathology of acute/primary and chronic HIV infection in humans, as well as simian immunodeficiency virus infection in rhesus macaques, according to the available literature.
format	article
author	Mahmoud Mohammad Yaseen Nizar Mohammad Abuharfeil Homa Darmani
author_facet	Mahmoud Mohammad Yaseen Nizar Mohammad Abuharfeil Homa Darmani
author_sort	Mahmoud Mohammad Yaseen
title	Myeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection
title_short	Myeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection
title_full	Myeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection
title_fullStr	Myeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection
title_full_unstemmed	Myeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection
title_sort	myeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection
publisher	The Royal Society
publishDate	2021
url	https://doaj.org/article/15c9867111ec4027b417fa6f0c846901
work_keys_str_mv	AT mahmoudmohammadyaseen myeloidderivedsuppressorcellsandthepathogenesisofhumanimmunodeficiencyvirusinfection AT nizarmohammadabuharfeil myeloidderivedsuppressorcellsandthepathogenesisofhumanimmunodeficiencyvirusinfection AT homadarmani myeloidderivedsuppressorcellsandthepathogenesisofhumanimmunodeficiencyvirusinfection
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Myeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection

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