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Mechanism of Rhinovirus Immunity and Asthma.
- Source :
-
Frontiers in immunology [Front Immunol] 2021 Oct 06; Vol. 12, pp. 731846. Date of Electronic Publication: 2021 Oct 06 (Print Publication: 2021). - Publication Year :
- 2021
-
Abstract
- 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.<br />Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.<br /> (Copyright © 2021 Yang, Mitländer, Vuorinen and Finotto.)
- Subjects :
- Adaptive Immunity
Animals
Asthma immunology
Asthma metabolism
Asthma physiopathology
Common Cold immunology
Common Cold metabolism
Common Cold physiopathology
Cytokines metabolism
Disease Progression
Host-Pathogen Interactions
Humans
Immunity, Innate
Immunocompromised Host
Lung immunology
Lung metabolism
Lung physiopathology
Rhinovirus pathogenicity
Signal Transduction
Asthma virology
Common Cold virology
Immune Evasion
Lung virology
Rhinovirus immunology
Subjects
Details
- Language :
- English
- ISSN :
- 1664-3224
- Volume :
- 12
- Database :
- MEDLINE
- Journal :
- Frontiers in immunology
- Publication Type :
- Academic Journal
- Accession number :
- 34691038
- Full Text :
- https://doi.org/10.3389/fimmu.2021.731846