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dc.contributor.authorWykes, Michelle N.
dc.contributor.authorLiu, Xue Q.
dc.contributor.authorJiang, Suhua
dc.contributor.authorHirunpetcharat, Chakrit
dc.contributor.authorGood, Michael F.
dc.description.abstractDendritic 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.en_US
dc.publisherAmerican Association of Immunologistsen_US
dc.publisher.placeUnited Statesen_US
dc.relation.ispartofjournalJournal of Immunologyen_US
dc.subject.fieldofresearchBiological Sciences not elsewhere classifieden_US
dc.titleSystemic tumour necrosis factor generated during lethal plasmodium infections impairs dendritic cell functionen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.rights.copyrightSelf-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.en_US
gro.hasfulltextNo Full Text
gro.griffith.authorGood, Michael F.

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