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dc.contributor.authorLoughland, Jessica R
dc.contributor.authorMinigo, Gabriela
dc.contributor.authorBurel, Julie
dc.contributor.authorTipping, Peta E
dc.contributor.authorPiera, Kim A
dc.contributor.authorAmante, Fiona H
dc.contributor.authorEngwerda, Christian R
dc.contributor.authorGood, Michael F
dc.contributor.authorDoolan, Denise L
dc.contributor.authorAnstey, Nicholas M
dc.contributor.authorMcCarthy, James S
dc.contributor.authorWoodberry, Tonia
dc.date.accessioned2018-08-27T03:00:03Z
dc.date.available2018-08-27T03:00:03Z
dc.date.issued2016
dc.identifier.issn0019-9567
dc.identifier.doi10.1128/IAI.01522-15
dc.identifier.urihttp://hdl.handle.net/10072/100027
dc.description.abstractDendritic cells (DCs) are sentinels of the immune system that uniquely prime naive cells and initiate adaptive immune responses. CD1c (BDCA-1) myeloid DCs (CD1c mDCs) highly express HLA-DR, have a broad Toll-like receptor (TLR) repertoire, and secrete immune modulatory cytokines. To better understand immune responses to malaria, CD1c mDC maturation and cytokine production were examined in healthy volunteers before and after experimental intravenous Plasmodium falciparum infection with 150- or 1,800-parasite-infected red blood cells (pRBCs). After either dose, CD1c mDCs significantly reduced HLA-DR expression in prepatent infections. Circulating CD1c mDCs did not upregulate HLA-DR after pRBC or TLR ligand stimulation and exhibited reduced CD86 expression. At peak parasitemia, CD1c mDCs produced significantly more tumor necrosis factor (TNF), whereas interleukin-12 (IL-12) production was unchanged. Interestingly, only the 1,800-pRBC dose caused a reduction in the circulating CD1c mDC count with evidence of apoptosis. The 1,800-pRBC dose produced no change in T cell IFN- or IL-2 production at peak parasitemia or at 3 weeks posttreatment. Overall, CD1c mDCs are compromised by P. falciparum exposure, with impaired HLA-DR and CD86 expression, and have an increased capacity for TNF but not IL-12 production. A first prepatent P. falciparum infection is sufficient to modulate CD1c mDC responsiveness, likely contributing to hampered effector T cell cytokine responses and assisting parasite immune evasion.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherAmerican Society for Microbiology
dc.relation.ispartofpagefrom1403
dc.relation.ispartofpageto1412
dc.relation.ispartofissue5
dc.relation.ispartofjournalInfection and Immunity
dc.relation.ispartofvolume84
dc.subject.fieldofresearchBiological Sciences not elsewhere classified
dc.subject.fieldofresearchBiological Sciences
dc.subject.fieldofresearchAgricultural and Veterinary Sciences
dc.subject.fieldofresearchMedical and Health Sciences
dc.subject.fieldofresearchcode069999
dc.subject.fieldofresearchcode06
dc.subject.fieldofresearchcode07
dc.subject.fieldofresearchcode11
dc.titleProfoundly Reduced CD1c+ Myeloid Dendritic Cell HLA-DR and CD86 Expression and Increased Tumor Necrosis Factor Production in Experimental Human Blood-Stage Malaria Infection
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2016 American Society for Microbiology. The attached file is reproduced here in accordance with the copyright policy of the publisher. Please refer to the journal's website for access to the definitive, published version.
gro.hasfulltextFull Text
gro.griffith.authorGood, Michael F.
gro.griffith.authorEngwerda, Christian R.


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