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    Allergen-specific CTL require perforin expression to suppress allergic airway inflammation.

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    Author
    Enomoto, N; Hyde, E; Ma, JZ-I; Yang, J; Forbes-Blom, E; Delahunt, B; Le Gros, G; Ronchese, F
    Date
    2012-02-15
    Source Title
    J Immunol
    Publisher
    The American Association of Immunologists
    University of Melbourne Author/s
    Ma, Joel
    Affiliation
    Microbiology And Immunology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Enomoto, 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.
    Access Status
    This item is currently not available from this repository
    URI
    http://hdl.handle.net/11343/32854
    DOI
    10.4049/jimmunol.1102699
    Description

    C1 - Journal Articles Refereed

    Abstract
    Allergen-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.
    Keywords
    Cellular Immunology; Immune System and Allergy

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