Mechanism of Rhinovirus Immunity and Asthma

The majority of asthma exacerbations in children are caused by Rhinovirus (RV), a positive sense single stranded RNA virus of the Picornavirus family. The host has developed virus defense mechanisms that are mediated by the upregulation of interferon-activated signaling. However, the virus evades th...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Zuqin Yang, Hannah Mitländer, Tytti Vuorinen, Susetta Finotto
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	asthma rhinovirus host defense immune evasion interferon type I Immunologic diseases. Allergy RC581-607
Acceso en línea:	https://doaj.org/article/c875f7c7393c470a93ae2cd6b5273862
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:c875f7c7393c470a93ae2cd6b5273862
record_format	dspace
spelling	oai:doaj.org-article:c875f7c7393c470a93ae2cd6b52738622021-11-16T11:33:21ZMechanism of Rhinovirus Immunity and Asthma1664-322410.3389/fimmu.2021.731846https://doaj.org/article/c875f7c7393c470a93ae2cd6b52738622021-10-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.731846/fullhttps://doaj.org/toc/1664-3224The majority of asthma exacerbations in children are caused by Rhinovirus (RV), a positive sense single stranded RNA virus of the Picornavirus family. The host has developed virus defense mechanisms that are mediated by the upregulation of interferon-activated signaling. However, the virus evades the immune system by inducing immunosuppressive cytokines and surface molecules like programmed cell death protein 1 (PD-1) and its ligand (PD-L1) on immunocompetent cells. Initially, RV infects epithelial cells, which constitute a physiologic mucosal barrier. Upon virus entrance, the host cell immediately recognizes viral components like dsRNA, ssRNA, viral glycoproteins or CpG-DNA by host pattern recognition receptors (PRRs). Activation of toll like receptors (TLR) 3, 7 and 8 within the endosome and through MDA-5 and RIG-I in the cytosol leads to the production of interferon (IFN) type I and other antiviral agents. Every cell type expresses IFNAR1/IFNAR2 receptors thus allowing a generalized antiviral activity of IFN type I resulting in the inhibition of viral replication in infected cells and preventing viral spread to non-infected cells. Among immune evasion mechanisms of the virus, there is downregulation of IFN type I and its receptor as well as induction of the immunosuppressive cytokine TGF-β. TGF-β promotes viral replication and is associated with induction of the immunosuppression signature markers LAP3, IDO and PD-L1. This article reviews the recent advances on the regulation of interferon type I expression in association with RV infection in asthmatics and the immunosuppression induced by the virus.Zuqin YangHannah MitländerTytti VuorinenSusetta FinottoFrontiers Media S.A.articleasthmarhinovirushost defenseimmune evasioninterferon type IImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	asthma rhinovirus host defense immune evasion interferon type I Immunologic diseases. Allergy RC581-607
spellingShingle	asthma rhinovirus host defense immune evasion interferon type I Immunologic diseases. Allergy RC581-607 Zuqin Yang Hannah Mitländer Tytti Vuorinen Susetta Finotto Mechanism of Rhinovirus Immunity and Asthma
description	The majority of asthma exacerbations in children are caused by Rhinovirus (RV), a positive sense single stranded RNA virus of the Picornavirus family. The host has developed virus defense mechanisms that are mediated by the upregulation of interferon-activated signaling. However, the virus evades the immune system by inducing immunosuppressive cytokines and surface molecules like programmed cell death protein 1 (PD-1) and its ligand (PD-L1) on immunocompetent cells. Initially, RV infects epithelial cells, which constitute a physiologic mucosal barrier. Upon virus entrance, the host cell immediately recognizes viral components like dsRNA, ssRNA, viral glycoproteins or CpG-DNA by host pattern recognition receptors (PRRs). Activation of toll like receptors (TLR) 3, 7 and 8 within the endosome and through MDA-5 and RIG-I in the cytosol leads to the production of interferon (IFN) type I and other antiviral agents. Every cell type expresses IFNAR1/IFNAR2 receptors thus allowing a generalized antiviral activity of IFN type I resulting in the inhibition of viral replication in infected cells and preventing viral spread to non-infected cells. Among immune evasion mechanisms of the virus, there is downregulation of IFN type I and its receptor as well as induction of the immunosuppressive cytokine TGF-β. TGF-β promotes viral replication and is associated with induction of the immunosuppression signature markers LAP3, IDO and PD-L1. This article reviews the recent advances on the regulation of interferon type I expression in association with RV infection in asthmatics and the immunosuppression induced by the virus.
format	article
author	Zuqin Yang Hannah Mitländer Tytti Vuorinen Susetta Finotto
author_facet	Zuqin Yang Hannah Mitländer Tytti Vuorinen Susetta Finotto
author_sort	Zuqin Yang
title	Mechanism of Rhinovirus Immunity and Asthma
title_short	Mechanism of Rhinovirus Immunity and Asthma
title_full	Mechanism of Rhinovirus Immunity and Asthma
title_fullStr	Mechanism of Rhinovirus Immunity and Asthma
title_full_unstemmed	Mechanism of Rhinovirus Immunity and Asthma
title_sort	mechanism of rhinovirus immunity and asthma
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/c875f7c7393c470a93ae2cd6b5273862
work_keys_str_mv	AT zuqinyang mechanismofrhinovirusimmunityandasthma AT hannahmitlander mechanismofrhinovirusimmunityandasthma AT tyttivuorinen mechanismofrhinovirusimmunityandasthma AT susettafinotto mechanismofrhinovirusimmunityandasthma
_version_	1718426574022246400

Mechanism of Rhinovirus Immunity and Asthma

Ejemplares similares