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dc.contributor.authorGood, Michaelen_US
dc.contributor.authorH. Amante, Fionaen_US
dc.contributor.authorLopez, Alejandroen_US
dc.contributor.authorM. Anstey, Nicholasen_US
dc.contributor.authorMinigo, Gabrielaen_US
dc.contributor.authorPiera, Kimen_US
dc.contributor.authorPinzon-Charry, Albertoen_US
dc.contributor.authorR. Entgwerda, Christianen_US
dc.contributor.authorS. McCarthy, Jamesen_US
dc.contributor.authorWoodberry, Toniaen_US
dc.date.accessioned2017-04-04T19:36:19Z
dc.date.available2017-04-04T19:36:19Z
dc.date.issued2012en_US
dc.date.modified2013-06-07T05:15:42Z
dc.identifier.issn00221899en_US
dc.identifier.doi10.1093/infdis/jis366en_US
dc.identifier.urihttp://hdl.handle.net/10072/47149
dc.description.abstractBackground. Dendritic cells (DCs) are highly specialized antigen-presenting cells that are crucial for initiation of immune responses. During naturally acquired malaria, DC number and function is reduced. Methods. The timing of, parasitemia threshold of, and contribution of apoptosis to DC loss were prospectively evaluated in 10 men after experimental challenge with approximately 1800 Plasmodium falciparum-parasitized red blood cells (pRBCs) and after drug cure initiated at a parasite level of =1000 parasites/mL. Results. The nadir levels of total, myeloid, and plasmacytoid DCs occurred 8 days after infection. DC loss was partially attributable to apoptosis, which was first detected on day 5 (median parasite level, 238 parasites/mL) and maximal at day 7. Remaining DCs exhibited a reduced ability to uptake particulate antigen. DC numbers recovered approximately 60 hours after antimalarial drug administration. There was no loss of DC number or function before or after drug cure in 5 men inoculated with <180 pRBCs and treated on day 6, when their parasite level was approximately 200 parasites/mL. Conclusions. Plasmodium causes DC loss in vivo, which is at least partially explained by apoptosis in response to blood-stage parasites. In primary infection, loss of DC number and function occurs early during the prepatent period and before or with onset of clinical symptoms. These findings may explain in part the inadequate development of immunity to blood-stage malaria infection.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_US
dc.languageEnglishen_US
dc.language.isoen_US
dc.publisherOxford University Pressen_US
dc.publisher.placeUnited Statesen_US
dc.relation.ispartofstudentpublicationNen_US
dc.relation.ispartofpagefrom333en_US
dc.relation.ispartofpageto340en_US
dc.relation.ispartofissue3en_US
dc.relation.ispartofjournalJournal of Infectious Diseasesen_US
dc.relation.ispartofvolume206en_US
dc.rights.retentionYen_US
dc.subject.fieldofresearchHost-Parasite Interactionsen_US
dc.subject.fieldofresearchImmunology not elsewhere classifieden_US
dc.subject.fieldofresearchcode060307en_US
dc.subject.fieldofresearchcode110799en_US
dc.titleLow-Level Plasmodium falciparum Blood-Stage Infection Causes Dendritic Cell Apoptosis and Dysfunction in Healthy Volunteersen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.date.issued2012
gro.hasfulltextNo Full Text


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