Mechanistically, although Plasmodium infection-induced type I IFNs have no appreciable direct effects on modulating Bcl-6+ Tfh development during malaria, they directly promote the accumulation and function of Plasmodium infection-induced T-bet+Blimp-1+ Tr1 cells that limit humoral immunity and parasite control via secretion of effector cytokines IL-10 and IFN-γ. This evidence concerns the gene BCL6 and malaria.