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dc.contributor.authorOwens, BMJ
dc.contributor.authorBeattie, L
dc.contributor.authorMoore, JWJ
dc.contributor.authorBrown, N
dc.contributor.authorMann, JL
dc.contributor.authorDalton, JE
dc.contributor.authorMaroof, A
dc.contributor.authorKaye, PM
dc.date.accessioned2020-12-18T04:13:42Z
dc.date.available2020-12-18T04:13:42Z
dc.date.issued2012-07-01
dc.identifierpii: PPATHOGENS-D-12-00308
dc.identifier.citationOwens, 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.
dc.identifier.issn1553-7374
dc.identifier.urihttp://hdl.handle.net/11343/256105
dc.description.abstractIL-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.
dc.languageEnglish
dc.publisherPUBLIC LIBRARY SCIENCE
dc.titleIL-10-Producing Th1 Cells and Disease Progression Are Regulated by Distinct CD11c(+) Cell Populations during Visceral Leishmaniasis
dc.typeJournal Article
dc.identifier.doi10.1371/journal.ppat.1002827
melbourne.affiliation.departmentMicrobiology and Immunology
melbourne.source.titlePLoS Pathogens
melbourne.source.volume8
melbourne.source.issue7
dc.rights.licenseCC BY
melbourne.elementsid1312276
melbourne.contributor.authorBeattie, Lynette
dc.identifier.eissn1553-7374
melbourne.accessrightsOpen Access


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