Publications & Reports

Plasmodium falciparum activates CD16+ dendritic cells to produce TNF and IL-10 in subpatent malaria.

Loughland JR, Woodberry T, Boyle MJ, Tipping PE, Piera KA, Amante FH, Kenangalem E, Price RN, Engwerda CR, Anstey NM, McCarthy JS, Minigo G
Menzies School of Health Research, Darwin, Australia and Charles Darwin University, Darwin, Australia.


The malaria causing parasite Plasmodium subverts host immune responses by several strategies including the modulation of dendritic cells (DCs). Here, we show P. falciparum skewed CD16+ DC cytokine responses towards 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 following induced P. falciparum infection in malaria-naive volunteers. CD16+ DCs underwent distinctive activation, with increased expression of maturation markers HLA-DR and CD86, enhanced TNF production and co-production of TNF/IL-10. In vitro re-stimulation 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. 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.

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  • Journal: The Journal of Infectious Diseases
  • Published: 29/01/2019
  • Volume: 219
  • Issue: 4
  • Pagination: 660-671