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dc.contributor.authorEnomoto, N
dc.contributor.authorHyde, E
dc.contributor.authorMa, JZ-I
dc.contributor.authorYang, J
dc.contributor.authorForbes-Blom, E
dc.contributor.authorDelahunt, B
dc.contributor.authorLe Gros, G
dc.contributor.authorRonchese, F
dc.date.available2014-05-22T07:16:19Z
dc.date.issued2012-02-15
dc.identifierpii: jimmunol.1102699
dc.identifier.citationEnomoto, N., Hyde, E., Ma, J. Z. -I., Yang, J., Forbes-Blom, E., Delahunt, B., Le Gros, G. & Ronchese, F. (2012). Allergen-specific CTL require perforin expression to suppress allergic airway inflammation.. J Immunol, 188 (4), pp.1734-1741. https://doi.org/10.4049/jimmunol.1102699.
dc.identifier.issn0022-1767
dc.identifier.urihttp://hdl.handle.net/11343/32854
dc.descriptionC1 - Journal Articles Refereed
dc.description.abstractAllergen-specific CTL have a protective effect on allergic airway inflammation, a function thought to be mediated by cytokines, especially IFN-γ. However, the contribution of cytotoxic function to this protective effect has not been investigated. We examined the contribution of cytotoxic function to the therapeutic effect of allergen-specific CTL in allergic airway inflammation. We used a murine model of allergic airway inflammation in which mice were sensitized to OVA and then challenged with the same Ag via the intranasal route. CTL were elicited in these mice by immunization with dendritic cells (DC) or by adoptive transfer of in vitro-activated CD8(+) T cells. Hallmark features of allergic asthma, such as infiltration of eosinophils in the bronchoalveolar lavage fluid and mucus production, were assessed. Suppression of allergic airway inflammation by allergen-specific CTL was critically dependent on the expression of perforin, a key component of the cytotoxic machinery. Both perforin-sufficient and perforin-deficient allergen-specific CTL were recovered from the lungs of allergen-sensitized mice and upregulated CD69 expression and secreted the cytokines IFN-γ and TNF-α upon intranasal allergen challenge. However, only perforin-sufficient CTL inhibited eosinophil infiltration in the airway, mucus production, and cytokine accumulation in the bronchoalveolar lavage fluid. Treatment with allergen-specific CTL, but not their perforin-deficient counterparts, was also associated with a decrease in the number of DC in the mediastinal lymph node. Our data suggest that the cytotoxic function of allergen-specific CD8(+) T cells is critical to their ability to moderate allergic airway inflammation.
dc.languageeng
dc.publisherThe American Association of Immunologists
dc.subjectCellular Immunology; Immune System and Allergy
dc.titleAllergen-specific CTL require perforin expression to suppress allergic airway inflammation.
dc.typeJournal Article
dc.identifier.doi10.4049/jimmunol.1102699
melbourne.peerreviewPeer Reviewed
melbourne.affiliationThe University of Melbourne
melbourne.affiliation.departmentMicrobiology And Immunology
melbourne.source.titleJ Immunol
melbourne.source.volume188
melbourne.source.issue4
melbourne.source.pages1734-1741
dc.research.codefor110704
dc.research.codeseo2008920108
melbourne.publicationid178320
melbourne.elementsid451916
melbourne.contributor.authorMa, Joel
dc.identifier.eissn1550-6606
melbourne.accessrightsThis item is currently not available from this repository


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