How malaria modulates memory: activation and dysregulation of B cells in Plasmodium infection

Trends Parasitol. 2013 May;29(5):252-62. doi: 10.1016/ Epub 2013 Apr 4.


Humoral immune responses play a major role in naturally acquired immunity to malaria, but are slow to develop and ineffectively maintained. Although this may be partially due to the complex nature of Plasmodium parasites and the high degree of antigenic variation, there is evidence that the parasite also actively alters B cell function. We integrate recent findings on the effect of Plasmodium falciparum (Pf) on B cells and the association of parasite exposure with altered B cell proportions, such as the expansion of atypical memory B cells. We propose a model of how the parasite may mediate these effects by direct interaction with B cells via the cysteine-rich interdomain region 1 α (CIDRα) of the erythrocyte membrane protein 1 (PfEMP1) and modulation of the host B cell activating factor (BAFF) immune pathway, and how this may compromise protective immune memory by interfering with B cell differentiation.

Publication types

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

MeSH terms

  • Antibodies, Protozoan / immunology
  • Antigenic Variation
  • Antigens, Protozoan / immunology
  • B-Cell Activating Factor / immunology*
  • B-Lymphocytes / immunology*
  • Cell Differentiation
  • Host-Parasite Interactions
  • Immunity, Humoral
  • Lymphocyte Activation
  • Malaria, Falciparum / immunology*
  • Malaria, Falciparum / parasitology
  • Models, Immunological
  • Plasmodium falciparum / immunology*
  • Plasmodium falciparum / physiology
  • Protozoan Proteins / immunology
  • Protozoan Proteins / metabolism*


  • Antibodies, Protozoan
  • Antigens, Protozoan
  • B-Cell Activating Factor
  • Protozoan Proteins
  • erythrocyte membrane protein 1, Plasmodium falciparum