B-cell memory in malaria: Myths and realities

Immunol Rev. 2020 Jan;293(1):57-69. doi: 10.1111/imr.12822. Epub 2019 Nov 16.


B-cell and antibody responses to Plasmodium spp., the parasite that causes malaria, are critical for control of parasitemia and associated immunopathology. Antibodies also provide protection to reinfection. Long-lasting B-cell memory has been shown to occur in response to Plasmodium spp. in experimental model infections, and in human malaria. However, there are reports that antibody responses to several malaria antigens in young children living with malaria are not similarly long-lived, suggesting a dysfunction in the maintenance of circulating antibodies. Some studies attribute this to the expansion of atypical memory B cells (AMB), which express multiple inhibitory receptors and activation markers, and are hyporesponsive to B-cell receptor (BCR) restimulation in vitro. AMB are also expanded in other chronic infections such as tuberculosis, hepatitis B and C, and HIV, as well as in autoimmunity and old age, highlighting the importance of understanding their role in immunity. Whether AMB are dysfunctional remains controversial, as there are also studies in other infections showing that AMB can produce isotype-switched antibodies and in mouse can contribute to protection against infection. In light of these controversies, we review the most recent literature on either side of the debate and challenge some of the currently held views regarding B-cell responses to Plasmodium infections.

Keywords: Plasmodium; classical and atypical memory B cells; long-lived plasma cells; malaria.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antibody Formation / immunology
  • Antigens, Protozoan / immunology
  • B-Lymphocytes / immunology*
  • B-Lymphocytes / metabolism
  • Clonal Anergy
  • Host-Parasite Interactions / immunology*
  • Humans
  • Immunologic Memory*
  • Malaria / immunology*
  • Malaria / metabolism
  • Malaria / parasitology
  • Plasmodium / immunology*
  • Receptors, Antigen, B-Cell / metabolism
  • Signal Transduction


  • Antigens, Protozoan
  • Receptors, Antigen, B-Cell