<i>Plasmodium</i> infection disrupts the T follicular helper cell response to heterologous immunization.

ABSTRACT: Naturally acquired immunity to malaria develops only after many years and repeated exposures, raising the question of whether Plasmodium parasites, the etiological agents of malaria, suppress the ability of dendritic cells (DCs) to activate optimal T cell responses. We demonstrated recently that B cells, rather than DCs, are the principal activators of CD4⁺ T cells in murine malaria. In the present study, we further investigated factors that might prevent DCs from priming Plasmodium-specific T helper cell responses. We found that DCs were significantly less efficient at taking up infected red blood cells (iRBCs) compared to soluble antigen, whereas B cells more readily bound iRBCs. To assess whether DCs retained the capacity to present soluble antigen during malari

SUBMITTER: Fontana MF 

PROVIDER: S-EPMC9886276 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature