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dc.contributor.authorAlyazidi, Raidan
dc.date.accessioned2016-01-19T18:51:18Z
dc.date.available2016-01-19T18:51:18Z
dc.date.issued2016-01-19T18:51:18Z
dc.identifier.urihttp://hdl.handle.net/10222/65338
dc.description.abstractRespiratory syncytial virus (RSV) is a major cause of infant bronchiolitis and the leading cause of their hospitalization worldwide. It is also linked to airway hyper-responsiveness. Mast cells are essential in allergies and the immune response to pathogens, and can produce various mediators that influence vascularity, bronchoconstriction, and immune cell recruitment to sites of infection. Since mast cells are abundant in the airways at the site of RSV infection, we examined the human mast cell response to RSV in vitro and the role type I interferons, major antiviral cytokines, play in such a response. Our data show that human mast cells responded to restricted RSV infection by producing pro-inflammatory chemokines and cytokines some of which were dependent on type I IFN response (CXCL10 and CCL4), while others were not (CCL5 and VEGF-A). Mast cell production of these mediators may enhance inflammation and effector cell recruitment during RSV disease.en_US
dc.language.isoenen_US
dc.subjectRESPIRATORY SYNCYTIAL VIRUSen_US
dc.subjectMAST CELL
dc.titlePRIMARY HUMAN MAST CELL ANTIVIRAL AND PRO-INFLAMMATORY RESPONSES TO RESPIRATORY SYNCYTIAL VIRUS (RSV)en_US
dc.typeThesis
dc.date.defence2014-08-14
dc.contributor.departmentMedical Sciencesen_US
dc.contributor.degreeMaster of Scienceen_US
dc.contributor.external-examinerDr. Craig McCormicken_US
dc.contributor.graduate-coordinatorDr. Jason Bermanen_US
dc.contributor.thesis-readerDr. Robert Andersonen_US
dc.contributor.thesis-readerDr. Scott Halperin
dc.contributor.thesis-readerDr. Thomas Issekutz
dc.contributor.thesis-supervisorDr. Jean Marshallen_US
dc.contributor.ethics-approvalReceiveden_US
dc.contributor.manuscriptsNot Applicableen_US
dc.contributor.copyright-releaseNot Applicableen_US
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