Profoundly reduced CD1c+ myeloid dendritic cell HLA-DR and CD86 expression and increased tumor necrosis factor production in experimental human blood-stage malaria infection

Loughland, Jessica R., Minigo, Gabriela, Burel, Julie, Tipping, Peta E., Piera, Kim A., Amante, Fiona H., Engwerda, Christian R., Good, Michael F., Doolan, Denise L., Anstey, Nicholas M., McCarthy, James S. and Woodberry, Tonia (2016) Profoundly reduced CD1c+ myeloid dendritic cell HLA-DR and CD86 expression and increased tumor necrosis factor production in experimental human blood-stage malaria infection. Infection and Immunity, 84 5: 1403-1412. doi:10.1128/IAI.01522-15

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Author Loughland, Jessica R.
Minigo, Gabriela
Burel, Julie
Tipping, Peta E.
Piera, Kim A.
Amante, Fiona H.
Engwerda, Christian R.
Good, Michael F.
Doolan, Denise L.
Anstey, Nicholas M.
McCarthy, James S.
Woodberry, Tonia
Title Profoundly reduced CD1c+ myeloid dendritic cell HLA-DR and CD86 expression and increased tumor necrosis factor production in experimental human blood-stage malaria infection
Formatted title
Profoundly reduced CD1c+ myeloid dendritic cell HLA-DR and CD86 expression and increased tumor necrosis factor production in experimental human blood-stage malaria infection
Journal name Infection and Immunity   Check publisher's open access policy
ISSN 1098-5522
0019-9567
Publication date 2016-05-01
Year available 2016
Sub-type Article (original research)
DOI 10.1128/IAI.01522-15
Open Access Status File (Publisher version)
Volume 84
Issue 5
Start page 1403
End page 1412
Total pages 10
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Collection year 2017
Language eng
Formatted abstract
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-γ 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.
Keyword Dendritic cells
DCs
CD1c+
Tumor Necrosis
Plasmodium falciparum
P. falciparum
Malaria
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
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