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    Induction of CD8(+) T lymphocytes by Salmonella typhimurium is independent of salmonella pathogenicity island 1-mediated host cell death

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    Author
    Wijburg, OLC; van Rooijen, N; Strugnell, RA
    Date
    2002-09-15
    Source Title
    JOURNAL OF IMMUNOLOGY
    Publisher
    AMER ASSOC IMMUNOLOGISTS
    University of Melbourne Author/s
    Wijburg, Odilia; Strugnell, Richard
    Affiliation
    Microbiology And Immunology
    Metadata
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    Document Type
    Journal Article
    Citations
    Wijburg, O. L. C., van Rooijen, N. & Strugnell, R. A. (2002). Induction of CD8(+) T lymphocytes by Salmonella typhimurium is independent of salmonella pathogenicity island 1-mediated host cell death. JOURNAL OF IMMUNOLOGY, 169 (6), pp.3275-3283. https://doi.org/10.4049/jimmunol.169.6.3275.
    Access Status
    This item is currently not available from this repository
    URI
    http://hdl.handle.net/11343/26606
    DOI
    10.4049/jimmunol.169.6.3275
    Description

    C1 - Journal Articles Refereed

    Abstract
    Salmonella are intracellular bacterial pathogens that reside and replicate inside macrophages, and attenuated strains of Salmonella typhimurium can be used to deliver heterologous Ags for MHC class I and/or MHC class II-restricted presentation. Recently, it was shown that invasion of macrophages by S. typhimurium may result in the death of host macrophages via a mechanism harboring features of apoptotic and necrotic cell death. However, it is unknown whether this bacterial-induced host cell death affects immunity. In addition, it has been hypothesized that macrophage death following infection with S. typhimurium and subsequent uptake of apoptotic cells by APC are fundamental to the induction of CTL responses. In this study we investigated the in vivo induction of Ag-specific CD8+ T lymphocyte responses and compared CD8+ T lymphocyte responses elicited with S. typhimurium strains carrying a mutation in their invA gene, and therefore an inability to induce Salmonella pathogenicity island 1 (SPI-1)-mediated macrophage death, with responses elicited by an attenuated deltaaroAD strain. Ag-specific CD8+ T lymphocyte responses were analyzed using IFN-gamma ELISPOT, tetramer binding, and in vivo and in vitro CTL assays. Our results showed that deltaaroAD and deltaaroADdeltainvA induced comparable levels of Ag-specific CD8+ T lymphocyte responses as well as protective, Ag-specific B and CD4+ T lymphocyte immunity. Furthermore, experiments in macrophage-depleted mice showed that CD8+ T lymphocyte responses were effectively induced in the absence of macrophages. Together, our results imply that in this infection model, SPI-1-mediated cell death does not affect the immunological defense response and is not important for the induction of CD8+ T lymphocyte responses.
    Keywords
    Humoral Immunology and Immunochemistry; Immune System and Allergy

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