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- Title
Plasmodium falciparum Activates CD16+ Dendritic Cells to Produce Tumor Necrosis Factor and Interleukin-10 in Subpatent Malaria.
- Authors
Loughland, Jessica R; Woodberry, Tonia; Boyle, Michelle J; Tipping, Peta E; Piera, Kim A; Amante, Fiona H; Kenangalem, Enny; Price, Ric N; Engwerda, Christian R; Anstey, Nicholas M; McCarthy, James S; Minigo, Gabriela
- Abstract
<bold>Background: </bold>The malaria causing parasite Plasmodium subverts host immune responses by several strategies including the modulation of dendritic cells (DCs).<bold>Methods: </bold>In this study, we show that Plasmodium falciparum skewed CD16+ DC cytokine responses towards interleukin (IL)-10 production in vitro, distinct to the cytokine profile induced by Toll-like receptor ligation. To determine CD16+ DC responsiveness in vivo, we assessed their function after induced P falciparum infection in malaria-naive volunteers.<bold>Results: </bold>CD16+ DCs underwent distinctive activation, with increased expression of maturation markers human leukocyte antigen (HLA)-DR and CD86, enhanced tumor necrosis factor (TNF) production, and coproduction of TNF/IL-10. In vitro restimulation with P falciparum further increased IL-10 production. In contrast, during naturally acquired malaria episode, CD16+ DCs showed diminished maturation, suggesting increased parasite burden and previous exposure influence DC subset function.<bold>Conclusions: </bold>These findings identify CD16+ DCs as the only DC subset activated during primary blood-stage human Plasmodium infection. As dual cytokine producers, CD16+ DCs contribute to inflammatory as well as regulatory innate immune processes.
- Publication
Journal of Infectious Diseases, 2018, Vol 218, Issue 6, pN.PAG
- ISSN
0022-1899
- Publication type
journal article
- DOI
10.1093/infdis/jiy555