Malaria is a major public health problem particularly in the tropics. It is caused by protozoan parasites belonging to the genus Plasmodium and is transmitted by Anopheles mosquitoes. Currently, strategies to control malaria include vector control measures, chemoprophylaxis, and efficient diagnosis and treatment. The availability of a highly efficacious malaria vaccine would greatly facilitate malaria control and possibly eradicate malaria. Efforts to design such malaria vaccines are underway but are greatly hampered by the poor understanding of how immune memory to malaria is generated and maintained. In this issue of the European Journal of Immunology, Wykes and colleagues [Eur. J. Immunol. 2012. 42: 3291-3301] demonstrate that experimental malaria infection lowers the expression of B-cell-activating factor in DCs, thereby compromising the ability of these DCs to stimulate memory B cells and sustain the survival of Ab-secreting cells. These findings provide potential clues in the quest for better understanding of immunity to malaria as discussed in this Commentary.
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