Abstract

Protective immunity against blood-stage Plasmodium infection and the disease malaria depends on antibodies secreted from high-affinity B cells selected during the germinal center (GC) response. The induction and stability of the GC response require the activation and direct cell-cell communication between parasite-specific CD4 helper T cells and B cells. However, cytokines secreted by helper T cells, B cells, and multiple other innate and adaptive immune cells also contribute to regulating the magnitude and protective functions of GC-dependent humoral immune responses. Here, we briefly review emerging data supporting the finding that specific cytokines can exhibit temporally distinct and context-dependent influences on the induction and maintenance of antimalarial humoral immunity.