Naturally acquired immunity to malaria develops only after many years of repeated exposure to Plasmodium parasites. Despite the key role that antibodies play in protection against malaria, the cellular processes underlying the slow acquisition of immunity are unclear. Children in high transmission settings that experience frequent malaria clinical episodes are characterized by a delayed development of parasite-specific memory B cells (MBC), suggesting that the inflammatory factors contributing to disease hinder these responses. We have recently addressed this hypothesis using a pre-clinical model of severe malaria and found that the same inflammatory pathways mediating disease syndromes impair germinal centre (GC) responses and the development of MBC and long-lived plasma cells required for antibody-mediated control of parasitemia. To further define molecular mechanisms by which malaria-driven inflammation impairs the induction of protective immunity, the development of GC responses to P. berghei ANKA was examined in mice deficient in the T helper 1-defining transcription factor T-bet in the T cell and B cell compatments. Genetic deletion of T-bet in T-bet^fl/flCD4^Cre mice significantly improved T follicular helper (Tfh) cell differentiation rates, which translated in enhanced GC and parasite-specific antibody responses to infection. Interestingly, malaria-driven T-bet expression not only affected the T cell compartment but also directly influenced B cell function, as infection of T-bet^fl/flCD23^Cre mice revealed that intrinsic expression of T-bet in mature B cells during infection influences the induction of humoral immunity by modulating the cellular dynamics of the GC reaction as well as the quality of the parasite-specific antibody response. Thus, these data suggest that inflammatory pathways mediated by T-bet in response to symptomatic malaria negatively impact the development of long-term humoral immunity by compromising T cell help for antibody formation and by directly influencing B cell activity.