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  • Immune Regulation during Experimental Visceral Leishmaniasis

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    Bunn_2017_01Thesis.pdf (4.699Mb)
    Author(s)
    Bunn, Patrick
    Primary Supervisor
    Good, Michael
    Other Supervisors
    Batzloff, Michael
    Engwerda, Christian
    Year published
    2014
    Metadata
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    Abstract
    Visceral Leishmaniasis (VL) is a chronic infectious disease caused by the protozoan parasites Leishmania donovani and L. infantum (chagasi) responsible for significant morbidity and mortality in the developing world. Transmitted by sand fly vectors, Leishmania parasites preferentially infect host macrophages throughout the viscera. Experimental L. donovani infection in genetically susceptible mice elicits a highly organ-specific outcome that mirrors much of the immunopathology observed in human VL patients. In this context, the liver is a site of an acute, resolving infection whereas parasite persistence is established in ...
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    Visceral Leishmaniasis (VL) is a chronic infectious disease caused by the protozoan parasites Leishmania donovani and L. infantum (chagasi) responsible for significant morbidity and mortality in the developing world. Transmitted by sand fly vectors, Leishmania parasites preferentially infect host macrophages throughout the viscera. Experimental L. donovani infection in genetically susceptible mice elicits a highly organ-specific outcome that mirrors much of the immunopathology observed in human VL patients. In this context, the liver is a site of an acute, resolving infection whereas parasite persistence is established in the chronically infected spleen. Generation of an effective immune response against infection requires IFNγ- and TNF-producing CD4+ T(h1) cells. Functional impairment of this pro-inflammatory subset is noted during chronic infection. Here, we describe 3 distinct pathways by which L. donovani promotes persistence within the host via the impairment of protective Th1 responses. IL-10 is a potent immunoregulatory cytokine well known for its T cell-modulatory activity. IL-10-producing CD4+ Th1 (Tr1) cells were found to contribute to much of the dysregulation observed during chronic L. donovani infection in C57BL/6 mice. While not influencing parasite control, Foxp3+ regulatory T(reg) cells were determined to be required for the induction of Tr1 cell populations during established infection. During chronic infection, however, Treg cells appeared to restrict the expansion of pathogenic Tr1 cells.
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    Thesis Type
    Thesis (PhD Doctorate)
    Degree Program
    Doctor of Philosophy (PhD)
    School
    Institute for Glycomics
    DOI
    https://doi.org/10.25904/1912/2731
    Copyright Statement
    The author owns the copyright in this thesis, unless stated otherwise.
    Item Access Status
    Public
    Subject
    Biological Sciences
    Medical and Health Sciences
    Visceral leishmaniasis (VL)
    Protozoan parasite Leishmania donovani
    Protozoan parasite L. infantum (chagasi)
    Experimental L. donovani infection
    Sand fly vectors
    Treg cells
    Publication URI
    http://hdl.handle.net/10072/366039
    Collection
    • Theses - Higher Degree by Research

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