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    IL-10-Producing Th1 Cells and Disease Progression Are Regulated by Distinct CD11c(+) Cell Populations during Visceral Leishmaniasis

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    Author
    Owens, BMJ; Beattie, L; Moore, JWJ; Brown, N; Mann, JL; Dalton, JE; Maroof, A; Kaye, PM
    Date
    2012-07-01
    Source Title
    PLoS Pathogens
    Publisher
    PUBLIC LIBRARY SCIENCE
    University of Melbourne Author/s
    Beattie, Lynette
    Affiliation
    Microbiology and Immunology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Owens, B. M. J., Beattie, L., Moore, J. W. J., Brown, N., Mann, J. L., Dalton, J. E., Maroof, A. & Kaye, P. M. (2012). IL-10-Producing Th1 Cells and Disease Progression Are Regulated by Distinct CD11c(+) Cell Populations during Visceral Leishmaniasis. PLOS PATHOGENS, 8 (7), https://doi.org/10.1371/journal.ppat.1002827.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/256105
    DOI
    10.1371/journal.ppat.1002827
    Abstract
    IL-10 is a critical regulatory cytokine involved in the pathogenesis of visceral leishmaniasis caused by Leishmania donovani and clinical and experimental data indicate that disease progression is associated with expanded numbers of CD4⁺ IFNγ⁺ T cells committed to IL-10 production. Here, combining conditional cell-specific depletion with adoptive transfer, we demonstrate that only conventional CD11c(hi) DCs that produce both IL-10 and IL-27 are capable of inducing IL-10-producing Th1 cells in vivo. In contrast, CD11c(hi) as well as CD11c(int/lo) cells isolated from infected mice were capable of reversing the host protective effect of diphtheria toxin-mediated CD11c⁺ cell depletion. This was reflected by increased splenomegaly, inhibition of NO production and increased parasite burden. Thus during chronic infection, multiple CD11c⁺ cell populations can actively suppress host resistance and enhance immunopathology, through mechanisms that do not necessarily involve IL-10-producing Th1 cells.

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