Malaria is an infectious disease of world-wide distribution, infecting millions of people each year. In regions of malaria endemicity, clinical immunity to infection takes many years of constant exposure to develop, and only partially protects the host against severe, symptomatic disease. These considerations highlight a defect in either the generation, maintenance or effector capacity of immune memory. In line with this hypothesis, recent evidence has suggested that inflammatory pathways mediating severe clinical malaria episodes also play a negative role in the induction of humoral immunity. IgM+ memory B cells (MBCs) are a recently characterised subgroup of memory cells. Unlike traditional IgG+ MBCs that preferentially differentiate into plasma cells (PCs) upon re-stimulation with antigen, IgM+ MBCs are proposed to have the additional capacity to initiate secondary germinal centre (GC) responses. The contribution of the IgM+ MBC compartment to humoral immunity in malaria has not yet been properly defined, and to address this question these cells were investigated using a murine model of severe malaria infection. My main results revealed that clinical episodes of malaria significantly reduce IgM+ MBC responses to infection. Adoptive transfer of IgM+ MBCs followed by re-infection of recipient mice with P. berghei ANKA support the concept of re-entry of these cells to GCs during recall. These results suggest the existence of multiple layers of MBCs, with distinct effector functions during recall responses that are induced by blood-stage malaria infections. It is conceivable that IgM+ MBCs may assist in the maintenance of anti-malarial immunity by remodelling their BC receptors within secondary GCs, thereby replenishing the IgG+ MBC pool to give rise to cells that can respond to antigenic variants of the parasite.