PMID- 26902728
OWN - NLM
STAT- MEDLINE
DCOM- 20170516
LR  - 20181202
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Print)
IS  - 0019-9567 (Linking)
VI  - 84
IP  - 5
DP  - 2016 May
TI  - Profoundly Reduced CD1c+ Myeloid Dendritic Cell HLA-DR and CD86 Expression and 
      Increased Tumor Necrosis Factor Production in Experimental Human Blood-Stage 
      Malaria Infection.
PG  - 1403-1412
LID - 10.1128/IAI.01522-15 [doi]
AB  - Dendritic 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-gamma 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.
CI  - Copyright (c) 2016, American Society for Microbiology. All Rights Reserved.
FAU - Loughland, Jessica R
AU  - Loughland JR
AD  - Menzies School of Health Research, Darwin, Australia, and Charles Darwin 
      University, Darwin, Australia jessica.loughland@menzies.edu.au.
FAU - Minigo, Gabriela
AU  - Minigo G
AD  - Menzies School of Health Research, Darwin, Australia, and Charles Darwin 
      University, Darwin, Australia.
FAU - Burel, Julie
AU  - Burel J
AD  - QIMR Berghofer Medical Research Institute and University of Queensland, Brisbane, 
      Australia.
FAU - Tipping, Peta E
AU  - Tipping PE
AD  - Menzies School of Health Research, Darwin, Australia, and Charles Darwin 
      University, Darwin, Australia.
FAU - Piera, Kim A
AU  - Piera KA
AD  - Menzies School of Health Research, Darwin, Australia, and Charles Darwin 
      University, Darwin, Australia.
FAU - Amante, Fiona H
AU  - Amante FH
AD  - QIMR Berghofer Medical Research Institute and University of Queensland, Brisbane, 
      Australia.
FAU - Engwerda, Christian R
AU  - Engwerda CR
AD  - QIMR Berghofer Medical Research Institute and University of Queensland, Brisbane, 
      Australia.
FAU - Good, Michael F
AU  - Good MF
AD  - Griffith University, Gold Coast, Queensland, Australia.
FAU - Doolan, Denise L
AU  - Doolan DL
AD  - QIMR Berghofer Medical Research Institute and University of Queensland, Brisbane, 
      Australia.
FAU - Anstey, Nicholas M
AU  - Anstey NM
AD  - Menzies School of Health Research, Darwin, Australia, and Charles Darwin 
      University, Darwin, Australia.
AD  - Royal Darwin Hospital, Darwin, Australia.
FAU - McCarthy, James S
AU  - McCarthy JS
AD  - QIMR Berghofer Medical Research Institute and University of Queensland, Brisbane, 
      Australia.
FAU - Woodberry, Tonia
AU  - Woodberry T
AD  - Menzies School of Health Research, Darwin, Australia, and Charles Darwin 
      University, Darwin, Australia.
LA  - eng
GR  - 095909/Wellcome Trust/United Kingdom
PT  - Journal Article
DEP - 20160422
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Antigens, CD1)
RN  - 0 (B7-2 Antigen)
RN  - 0 (CD1C protein, human)
RN  - 0 (CD86 protein, human)
RN  - 0 (Glycoproteins)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (TNF protein, human)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adult
MH  - Antigens, CD1/*analysis
MH  - B7-2 Antigen/*analysis
MH  - Cohort Studies
MH  - Dendritic Cells/*chemistry/*immunology
MH  - Female
MH  - Glycoproteins/*analysis
MH  - HLA-DR Antigens/*analysis
MH  - Healthy Volunteers
MH  - Humans
MH  - Malaria, Falciparum/*pathology
MH  - Male
MH  - Plasmodium falciparum/immunology
MH  - Tumor Necrosis Factor-alpha/*metabolism
MH  - Young Adult
PMC - PMC4862702
EDAT- 2016/02/24 06:00
MHDA- 2017/05/17 06:00
PMCR- 2016/10/22
CRDT- 2016/02/24 06:00
PHST- 2015/12/15 00:00 [received]
PHST- 2016/02/13 00:00 [accepted]
PHST- 2016/02/24 06:00 [entrez]
PHST- 2016/02/24 06:00 [pubmed]
PHST- 2017/05/17 06:00 [medline]
PHST- 2016/10/22 00:00 [pmc-release]
AID - IAI.01522-15 [pii]
AID - 01522-15 [pii]
AID - 10.1128/IAI.01522-15 [doi]
PST - epublish
SO  - Infect Immun. 2016 Apr 22;84(5):1403-1412. doi: 10.1128/IAI.01522-15. Print 2016 
      May.