Malaria is a significant cause of mortality and morbidity globally. Plasmodium falciparum and P. vivax are the parasite species responsible for the majority of malaria cases. Protective immunity to both P. falciparum and P. vivax is mediated by antibodies. Induction of protective antibodies is driven by CD4 T follicular helper cells which activate B cells during infection. To date, there is only a single study of Tfh cells during infection for P.vivax and P. falciparum, but no study has directly investigated the influence of parasite each species on Tfh cell responses during malaria in humans.
We assessed Tfh cell responses in adults with either uncomplicated Plasmodium falciparum (n=8) or Plasmodium vivax (n=8) malaria compared to healthy uninfected endemic controls (n=5). Tfh cell responses were measured ex vivo by flow cytometry and functional capacity measured by intracellular staining of cytokines produced following PMA/Ionomycin stimulation.
We observed significant increase in Tfh cells numbers and activation of Tfh cells across species. Both Th1 and Th2 – Tfh cell subsets are activated by both species. However, there are no differences in the Tfh subset distribution and cytokine profiles between species.
Our data shows that Tfh cells are activated in P falciparum and P.vivax infections but the parasite species does not influence their activation and function during infection. These findings provide insights into the influence of malaria parasite species on Tfh cell responses and warrants further assessment for strategies targeting Tfh cell responses to improve vaccine efficacy.