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dc.contributor.authorWebby, RJ
dc.contributor.authorAndreansky, S
dc.contributor.authorStambas, J
dc.contributor.authorRehg, JE
dc.contributor.authorWebster, RG
dc.contributor.authorDoherty, PC
dc.contributor.authorTurner, SJ
dc.date.available2014-05-21T19:38:58Z
dc.date.issued2003-06-10
dc.identifierpii: 1232449100
dc.identifier.citationWebby, R. J., Andreansky, S., Stambas, J., Rehg, J. E., Webster, R. G., Doherty, P. C. & Turner, S. J. (2003). Protection and compensation in the influenza virus-specific CD8+ T cell response. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 100 (12), pp.7235-7240. https://doi.org/10.1073/pnas.1232449100.
dc.identifier.issn0027-8424
dc.identifier.urihttp://hdl.handle.net/11343/26583
dc.descriptionC1 - Journal Articles Refereed
dc.description.abstractInfluenza virus-specific CD8+ T cells generally recognize peptides derived from conserved, internal proteins that are not subject to antibody-mediated selection pressure. Prior exposure to any one influenza A virus (H1N1) can prime for a secondary CD8+ T cell response to a serologically different influenza A virus (H3N2). The protection afforded by this recall of established CD8+ T cell memory, although limited, is not negligible. Key characteristics of primary and secondary influenza-specific host responses are probed here with recombinant viruses expressing modified nucleoprotein (NP) and acid polymerase (PA) genes. Point mutations were introduced into the epitopes derived from the NP and PA such that they no longer bound the presenting H2Db MHC class I glycoprotein, and reassortant H1N1 and H3N2 viruses were made by reverse genetics. Conventional (C57BL/6J, H2b, and Ig+/+) and Ig-/- (muMT) mice were more susceptible to challenge with the single NP [HKx31 influenza A virus (HK)-NP] and PA (HK-PA) mutants, but unlike the Ig-/- mice, Ig+/+ mice were surprisingly resistant to the HK-NP/-PA double mutant. This virus was found to promote an enhanced IgG response resulting, perhaps, from the delayed elimination of antigen-presenting cells. Antigen persistence also could explain the increase in size of the minor KbPB1703 CD8+ T cell population in mice infected with the mutant viruses. The extent of such compensation was always partial, giving the impression that any virus-specific CD8+ T cell response operates within constrained limits. It seems that the relationship between protective humoral and cellular immunity is neither simple nor readily predicted.
dc.formatapplication/pdf
dc.languageEnglish
dc.publisherNATL ACAD SCIENCES
dc.subjectCellular Immunology; Immune System and Allergy
dc.titleProtection and compensation in the influenza virus-specific CD8+ T cell response
dc.typeJournal Article
dc.identifier.doi10.1073/pnas.1232449100
melbourne.peerreviewPeer Reviewed
melbourne.affiliationThe University of Melbourne
melbourne.affiliation.departmentMicrobiology And Immunology
melbourne.source.titlePROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
melbourne.source.volume100
melbourne.source.issue12
melbourne.source.pages7235-7240
melbourne.publicationid18349
melbourne.elementsid257015
melbourne.openaccess.pmchttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC165859
melbourne.contributor.authorStambas, John
melbourne.contributor.authorDoherty, Peter
melbourne.contributor.authorTurner, Stephen
dc.identifier.eissn1091-6490
melbourne.accessrightsAccess this item via the Open Access location


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