dc.contributor.authorPiva, L.
dc.contributor.authorTetlak, P.
dc.contributor.authorClaser, C.
dc.contributor.authorKarjalainen, K.
dc.contributor.authorRenia, L.
dc.contributor.authorRuedl, Christiane
dc.identifier.citationPiva, L., Tetlak, P., Claser, C., Karjalainen, K., Renia, L.,& Ruedl, C. (2012). Cutting edge : Clec9A+ dendritic cells mediate the development of experimental cerebral Malaria. The journal of immunology, 189(3), 1128-1132.en_US
dc.description.abstractPlasmodium infections trigger strong innate and acquired immune responses, which can lead to severe complications, including the most feared and often fatal cerebral malaria (CM). To begin to dissect the roles of different dendritic cell (DC) subsets in Plasmodium-induced pathology, we have generated a transgenic strain, Clec9A-diphtheria toxin receptor that allows us to ablate in vivo Clec9A+ DCs. Specifically, we have analyzed the in vivo contribution of this DC subset in an experimental CM model using Plasmodium berghei, and we provide strong evidence that the absence of this DC subset resulted in complete resistance to experimental CM. This was accompanied with dramatic reduction of brain CD8 + T cells, and those few cerebral CD8 + T cells present had a less activated phenotype, unlike their wildtype counterparts that expressed IFN-γ and especially granzyme B. This almost complete absence of local cellular responses was also associated with reduced parasite load in the brain.en_US
dc.description.sponsorshipNMRC (Natl Medical Research Council, S’pore)
dc.relation.ispartofseriesThe journal of immunologyen_US
dc.subjectDRNTU::Science::Biological sciences
dc.titleCutting edge : Clec9A+ dendritic cells mediate the development of experimental cerebral Malariaen_US
dc.typeJournal Article
dc.contributor.schoolSchool of Biological Sciencesen_US

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