Rhinovirus has the unique ability to directly activate human T cells in vitro

Ilarraza, Ramses; Wu, Yingqi; Skappak, Christopher; Ajamian, Farnam; Adamko, Darryl J.

doi:10.1016/j.jaci.2012.11.041

Cited by 25 publications

(19 citation statements)

References 68 publications

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“…It is already known that RV could bypass antigen presentation and could directly infect T cells. 37 We thus next ask whether the RV targets Th17 cells in asthma. We found that infection of lung CD4 þ T cells with RV1b resulted in a significant reduction of IL-17A.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, it could also be demonstrated that RV, in contrast to RSV, is able to directly infect and activate CD4 þ T cells. [35][36][37] To address the role of IL-17A during RV infection in asthma, we infected lung CD4 þ T cells obtained from OVA-sensitized wild type and Il17a ( À / À ) mice with RV1b and cultured them for 24 h (Figure 3a). By analyzing these cells we could observe that Il17a-deficient lung CD4 þ T cells from naïve mice express significantly more Ldlr than the corresponding wt mice.…”

Section: Rv1b Infection Downregulated Il-17a In Lung Cd4 þ T Cells Ismentioning

confidence: 99%

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Rhinovirus inhibits IL-17A and the downstream immune responses in allergic asthma

et al. 2016

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The proinflammatory cytokine interleukin-17A (IL-17A) is known to mediate antimicrobial activity, but its role during rhinovirus (RV) infections and in asthma needs further investigation. Therefore, we addressed the role of IL-17A during allergic asthma and antiviral immune response in human and murine immunocompetent cells. In this study we found that asthmatic children with a RV infection in their upper airways have upregulated mRNA levels of the antiviral cytokine interferon type I (IFN)-β and the transcription factor T-box 21 (TBX21) and reduced levels of IL-17A protein in their peripheral blood mononuclear cells (PBMCs). We also found that IL-17A inhibited RV1b replication in infected human lung epithelial cells A549. Furthermore, by using gene array analysis we discovered that targeted deletion of Il17a in murine lung CD4(+) T cells impaired Oas1g mRNA downstream of Ifnβ, independently from RV infection. Additionally, in PBMCs of children with a RV infection in their nasalpharyngeal fluid OAS1 gene expression was found downregulated. Finally RV1b inhibited IL-17A production in lung CD4(+) T cells in a setting of experimental asthma. These results indicate that the RV1b inhibits IL-17A in T helper type 17 cells and IL-17A clears RV1b infection in epithelial cells. In both cases IL-17A contributes to fend off RV1b infection by inducing genes downstream of interferon type I pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Rv1b Infection Downregulated Il-17a In Lung Cd4 þ T Cells Ismentioning

confidence: 99%

Rhinovirus inhibits IL-17A and the downstream immune responses in allergic asthma

et al. 2016

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“…Certain strains of RV have been demonstrated to have the unique ability to bypass antigen presentation and directly infect and activate CD4 1 and CD8 1 T cells. This could explain the strong association of rhinovirus with exacerbation of airway diseases and may have relevance to early-life altered immune response to RV that could be strain specific rather than illness severity specific (104). RV infection has also been shown to increase deposition of the extracellular matrix proteins collagen and endothelial growth factor in cultured human bronchial ECs possibly mediated through TLRs.…”

Section: Biologic Mechanisms Through Which Respiratory Viral Infectiomentioning

confidence: 98%

Toward Primary Prevention of Asthma. Reviewing the Evidence for Early-Life Respiratory Viral Infections as Modifiable Risk Factors to Prevent Childhood Asthma

Feldman

Moore

et al. 2015

Am J Respir Crit Care Med

167

172

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A first step in primary disease prevention is identifying common, modifiable risk factors that contribute to a significant proportion of disease development. Infant respiratory viral infection and childhood asthma are the most common acute and chronic diseases of childhood, respectively. Common clinical features and links between these diseases have long been recognized, with early-life respiratory syncytial virus (RSV) and rhinovirus (RV) lower respiratory tract infections (LRTIs) being strongly associated with increased asthma risk. However, there has long been debate over the role of these respiratory viruses in asthma inception. In this article, we systematically review the evidence linking early-life RSV and RV LRTIs with asthma inception and whether they could therefore be targets for primary prevention efforts.

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“…RV‐specific T cells can be activated by either serotype‐specific or shared viral epitopes from different RV serotypes contributing to antiviral activity and airway inflammation . Rhinovirus belonging to the major‐group RV has been shown to directly infect and activate human T cells without intervention of antigen‐presenting cells …”

Section: Rhinovirusesmentioning

confidence: 99%

Rhinovirus and preschool wheeze

Stenberg‐Hammar

Hedlin

Söderhäll

2017

Pediatric Allergy Immunology

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Rhinovirus (RV) known as the common cold virus generally only causes a mild upper respiratory infection, but severe lower respiratory symptoms have been associated with RV infections especially in asthmatic individuals. Wheezing is a symptom of airway obstruction, and preschool children wheezing with RV have been associated with increased risk of asthma at school age. There are, however, conflicting opinions as to whether there are differences in response to RV infection or whether wheezing with RV reveals a preexisting impairment that promotes asthma mainly in predisposed children. The advent of molecular diagnostics to detect respiratory viruses has led to new insights into the role of RV infections. This review will discuss recent information concerning the role of RV as an important respiratory pathogen related to early onset wheeze and exacerbation of established asthma in preschool children.

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Rhinovirus has the unique ability to directly activate human T cells in vitro

Cited by 25 publications

References 68 publications

Rhinovirus inhibits IL-17A and the downstream immune responses in allergic asthma

Rhinovirus inhibits IL-17A and the downstream immune responses in allergic asthma

Toward Primary Prevention of Asthma. Reviewing the Evidence for Early-Life Respiratory Viral Infections as Modifiable Risk Factors to Prevent Childhood Asthma

Rhinovirus and preschool wheeze

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