Adaptive immunity to Plasmodium blood stages

Adaptive immune responses to Plasmodium infection develop over many years in malaria-exposed individuals. Natural immunity is capable of reducing the severity of infection and lowering overall parasitemia but does not block infection. Moreover, there is some evidence that clinical immunity is short-lived as individuals who leave endemic areas become susceptible to disease once more. A proper understanding of the adaptive immune response is important to the pathology-causing blood-stage infection, not least because the induction of anti-disease immunity is one possible Plasmodium vaccination strategy. Nonetheless, the correlates of protective immunity are incompletely understood, and the reasons for the slow and incomplete development of immunity are unclear. Here we briefly review what is known about the roles of antibodies, B cells and T cells, in mediating protection. We examine which parasite antigens are likely to be the targets of protective antibodies. Finally we discuss why better, sterilizing, immunity to malaria does not develop with an emphasis on the fate of memory B and T cell populations in infection.