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  • Systemic tumour necrosis factor generated during lethal plasmodium infections impairs dendritic cell function

    Author(s)
    Wykes, Michelle N.
    Liu, Xue Q.
    Jiang, Suhua
    Hirunpetcharat, Chakrit
    Good, Michael F.
    Griffith University Author(s)
    Good, Michael F.
    Year published
    2007
    Metadata
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    Abstract
    Dendritic cells (DCs) initiate innate and adaptive immune responses including those against malaria. Although several studies have shown that DC function is normal during malaria, other studies have shown compromised function. To establish why these studies had different findings, we examined DCs from mice infected with two lethal species of parasite, Plasmodium berghei or P. vinckei, and compared them to DCs from nonlethal P. yoelii 17XNL or P. chabaudi infections. These studies found that DCs from only the lethal infections became uniformly mature 7 days after infection and were functionally impaired as they were unable ...
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    Dendritic cells (DCs) initiate innate and adaptive immune responses including those against malaria. Although several studies have shown that DC function is normal during malaria, other studies have shown compromised function. To establish why these studies had different findings, we examined DCs from mice infected with two lethal species of parasite, Plasmodium berghei or P. vinckei, and compared them to DCs from nonlethal P. yoelii 17XNL or P. chabaudi infections. These studies found that DCs from only the lethal infections became uniformly mature 7 days after infection and were functionally impaired as they were unable to endocytose latex particles, secrete IL-12, or present OVA to transgenic OTII T cells. These changes coincided with a peak in levels of systemic TNF-a. Because TNF-a is known to mature DCs, we used TNF-KO mice to determine the role of this cytokine in the loss of DC function. In the TNF-KO mice, phenotype, Ag presentation, and IL-12 secretion by DCs were restored to normal following both lethal infections. This study shows that the systemic production of TNF-a contributes to poor DC function during lethal infections. These studies may explain, at least in part, immunosuppression that is associated with malaria.
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    Journal Title
    Journal of Immunology
    Volume
    179
    Issue
    6
    DOI
    https://doi.org/10.4049/jimmunol.179.6.3982
    Copyright Statement
    Self-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.
    Subject
    Biological Sciences not elsewhere classified
    Immunology
    Publication URI
    http://hdl.handle.net/10072/143691
    Collection
    • Journal articles

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