Rhinovirus has the unique ability to directly activate human T cells in vitro
Identifieur interne : 001270 ( Main/Exploration ); précédent : 001269; suivant : 001271Rhinovirus has the unique ability to directly activate human T cells in vitro
Auteurs : Ramses Ilarraza [Canada] ; YINGQI WU [Canada] ; Christopher D. Skappak [Canada] ; Farnam Ajamian [Canada] ; David Proud [Canada] ; Darryl J. Adamko [Canada]Source :
- Journal of allergy and clinical immunology [ 0091-6749 ] ; 2013.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme, Immunologie.
English descriptors
- KwdEn :
Abstract
Background: Rhinovirus infection is a leading cause of exacerbation of airway diseases. We hypothesize that airway viruses activate inflammatory cells, inducing airway dysfunction. We have previously shown that airway viruses can induce eosinophil degranulation when cocultured with T cells and monocyte-derived dendritic cells (moDCs). These findings suggested that antigen presentation was important for T-cell activation. Objective: Given the clinical importance of rhinovirus, we sought to determine whether it had any unique abilities to activate inflammatory cells compared with another common virus, such as respiratory syncytial virus (RSV). Methods: We cocultured combinations of human leukocytes (T cells, moDCs, and eosinophils) with each virus. Using assays of BrdU incorporation, flow cytometry, and ELISA, we measured T-cell activation, rhinovirus expression, T-cell death, and eosinophil cysteinyl leukotriene release. Results: In contrast to RSV, rhinovirus induced T-cell activation without the involvement of moDCs. Without moDCs, rhinovirus induced T-cell proliferation of both CD4 and CD8+ cells, cytokine production, and ultimately, eosinophil stimulation. Although chloroquine inhibited RSV-induced activation of T cells through moDCs, rhinovirus was not inhibited; UV inactivation did block the rhinovirus effect. We also found that T cells could be infected by rhinovirus in vitro and within human nasal explant tissue. Although Toll-like receptors did not appear to be involved in T-cell activation, antagonists of Jun N-terminal kinase and nuclear factor κB did inhibit T-cell responses to rhinovirus. Conclusion: Rhinovirus has the unique ability to bypass antigen presentation and directly infect and activate human T cells. This could explain the strong association of rhinovirus with exacerbation of airway diseases.
Affiliations:
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Skappak</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Pediatrics, University of Alberta</s1><s2>Edmonton</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Edmonton</wicri:noRegion></affiliation></author><author><name sortKey="Ajamian, Farnam" sort="Ajamian, Farnam" uniqKey="Ajamian F" first="Farnam" last="Ajamian">Farnam Ajamian</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Medicine, University of Alberta</s1><s2>Edmonton</s2><s3>CAN</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Edmonton</wicri:noRegion></affiliation></author><author><name sortKey="Proud, David" sort="Proud, David" uniqKey="Proud D" first="David" last="Proud">David Proud</name><affiliation wicri:level="4"><inist:fA14 i1="04"><s1>Department of Physiology and Pharmacology, University of Calgary</s1><s3>CAN</s3><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Calgary</settlement><region type="state">Alberta</region></placeName><orgName type="university">Université de Calgary</orgName></affiliation></author><author><name sortKey="Adamko, Darryl J" sort="Adamko, Darryl J" uniqKey="Adamko D" first="Darryl J." last="Adamko">Darryl J. Adamko</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Pediatrics, University of Alberta</s1><s2>Edmonton</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Edmonton</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Medicine, University of Alberta</s1><s2>Edmonton</s2><s3>CAN</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Edmonton</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Pediatrics, College of Medicine, University of Saskatchewan</s1><s2>Saskatoon</s2><s3>CAN</s3><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Saskatoon</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Journal of allergy and clinical immunology</title><title level="j" type="abbreviated">J. allergy clin. immunol.</title><idno type="ISSN">0091-6749</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of allergy and clinical immunology</title><title level="j" type="abbreviated">J. allergy clin. immunol.</title><idno type="ISSN">0091-6749</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Asthma</term><term>Exacerbation</term><term>Human</term><term>Human respiratory syncytial virus</term><term>Immunology</term><term>Immunopathology</term><term>In vitro</term><term>Respiratory tract</term><term>Rhinovirus</term><term>T-Lymphocyte</term><term>Viral disease</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Asthme</term><term>Rhinovirus</term><term>Homme</term><term>Lymphocyte T</term><term>In vitro</term><term>Virose</term><term>Virus respiratoire syncytial humain</term><term>Voie respiratoire</term><term>Immunologie</term><term>Immunopathologie</term><term>Exacerbation</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term><term>Immunologie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background: Rhinovirus infection is a leading cause of exacerbation of airway diseases. We hypothesize that airway viruses activate inflammatory cells, inducing airway dysfunction. We have previously shown that airway viruses can induce eosinophil degranulation when cocultured with T cells and monocyte-derived dendritic cells (moDCs). These findings suggested that antigen presentation was important for T-cell activation. Objective: Given the clinical importance of rhinovirus, we sought to determine whether it had any unique abilities to activate inflammatory cells compared with another common virus, such as respiratory syncytial virus (RSV). Methods: We cocultured combinations of human leukocytes (T cells, moDCs, and eosinophils) with each virus. Using assays of BrdU incorporation, flow cytometry, and ELISA, we measured T-cell activation, rhinovirus expression, T-cell death, and eosinophil cysteinyl leukotriene release. Results: In contrast to RSV, rhinovirus induced T-cell activation without the involvement of moDCs. Without moDCs, rhinovirus induced T-cell proliferation of both CD4 and CD8<sup>+</sup> cells, cytokine production, and ultimately, eosinophil stimulation. Although chloroquine inhibited RSV-induced activation of T cells through moDCs, rhinovirus was not inhibited; UV inactivation did block the rhinovirus effect. We also found that T cells could be infected by rhinovirus in vitro and within human nasal explant tissue. Although Toll-like receptors did not appear to be involved in T-cell activation, antagonists of Jun N-terminal kinase and nuclear factor κB did inhibit T-cell responses to rhinovirus. Conclusion: Rhinovirus has the unique ability to bypass antigen presentation and directly infect and activate human T cells. This could explain the strong association of rhinovirus with exacerbation of airway diseases.</div></front></TEI><affiliations><list><country><li>Canada</li></country><region><li>Alberta</li></region><settlement><li>Calgary</li></settlement><orgName><li>Université de Calgary</li></orgName></list><tree><country name="Canada"><noRegion><name sortKey="Ilarraza, Ramses" sort="Ilarraza, Ramses" uniqKey="Ilarraza R" first="Ramses" last="Ilarraza">Ramses Ilarraza</name></noRegion><name sortKey="Adamko, Darryl J" sort="Adamko, Darryl J" uniqKey="Adamko D" first="Darryl J." last="Adamko">Darryl J. Adamko</name><name sortKey="Adamko, Darryl J" sort="Adamko, Darryl J" uniqKey="Adamko D" first="Darryl J." last="Adamko">Darryl J. Adamko</name><name sortKey="Adamko, Darryl J" sort="Adamko, Darryl J" uniqKey="Adamko D" first="Darryl J." last="Adamko">Darryl J. Adamko</name><name sortKey="Ajamian, Farnam" sort="Ajamian, Farnam" uniqKey="Ajamian F" first="Farnam" last="Ajamian">Farnam Ajamian</name><name sortKey="Proud, David" sort="Proud, David" uniqKey="Proud D" first="David" last="Proud">David Proud</name><name sortKey="Skappak, Christopher D" sort="Skappak, Christopher D" uniqKey="Skappak C" first="Christopher D." last="Skappak">Christopher D. Skappak</name><name sortKey="Yingqi Wu" sort="Yingqi Wu" uniqKey="Yingqi Wu" last="Yingqi Wu">YINGQI WU</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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