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dc.contributor.authorCole, Charles Josh
dc.date.accessioned2014-03-04T20:23:44Z
dc.date.available2014-03-04T20:23:44Z
dc.date.issued2011-12
dc.identifier.othercole_charles_j_201112_ms
dc.identifier.urihttp://purl.galileo.usg.edu/uga_etd/cole_charles_j_201112_ms
dc.identifier.urihttp://hdl.handle.net/10724/27687
dc.description.abstractInfluenza remains a public health priority in the U.S. particularly with new, rapidly emerging strains of the virus. Natural Killer (NK) cells are activated after contacting influenza infected epithelial cell and are crucial for viral clearance. Understanding the mechanisms of the NK cell response to influenza could illuminate ways to augment the non-specific immunity, which could provide rapid, short-term protection. We hypothesize that NK cells are dependent on direct IL-15/IL-15Rα signaling for recruitment to the lung airways after an influenza infection. Here, we examined the relationship between NK cell recruitment and Interleukin-15 (IL-15) at the site of influenza infection. We show that NK cell recruitment is dependent on the local expression of IL-15. In IL-15-ablated models, fewer NK cells migrated to the site of infection, whereas treatment with soluble IL-15 led to increased recruitment of NK cells to the lung airways. Altogether, these data suggest an important role for IL-15 in the recruitment of NK cell responses to influenza, while also revealing a potential therapeutic use of for IL-15.
dc.languageeng
dc.publisheruga
dc.rightspublic
dc.subjectInfluenza virus A
dc.subjectNatural Killer Cell
dc.subjectIL-15, IL-15Rα
dc.subjectTrafficking
dc.subjectInnate Immunity
dc.titleRole of IL-15 in Natural Killer cell responses to influenza infection
dc.typeThesis
dc.description.degreeMS
dc.description.departmentCellular Biology
dc.description.majorCellular Biology
dc.description.advisorKim Klonowski
dc.description.committeeKim Klonowski
dc.description.committeeS. Mark Tompkins
dc.description.committeeRick Tarleton


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