The Breadth, but Not the Magnitude, of Circulating Memory B Cell Responses to P. falciparum Increases with Age/Exposure in an Area of Low Transmission

Medical Research Council Laboratories, Fajara, Banjul, The Gambia.
PLoS ONE (Impact Factor: 3.23). 10/2011; 6(10):e25582. DOI: 10.1371/journal.pone.0025582
Source: PubMed


Malaria caused by Plasmodium falciparum remains a major cause of death in sub-Saharan Africa. Immunity against symptoms of malaria requires repeated exposure, suggesting either that the parasite is poorly immunogenic or that the development of effective immune responses to malaria may be impaired.
We carried out two age-stratified cross-sectional surveys of anti-malarial humoral immune responses in a Gambian village where P. falciparum malaria transmission is low and sporadic. Circulating antibodies and memory B cells (MBC) to four malarial antigens were measured using ELISA and cultured B cell ELISpot.
The proportion of individuals with malaria-specific MBC and antibodies, and the average number of antigens recognised by each individual, increased with age but the magnitude of these responses did not. Malaria-specific antibody levels did not correlate with either the prevalence or median number of MBC, indicating that these two assays are measuring different aspects of the humoral immune response. Among those with immunological evidence of malaria exposure (defined as a positive response to at least one malarial antigen either by ELISA or ELISPOT), the median number of malaria-specific MBC was similar to median numbers of diphtheria-specific MBC, suggesting that the circulating memory cell pool for malaria antigens is of similar size to that for other antigens.

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    • "Similarly, memory B cells specific for one or more malarial antigens have been reported to be maintained for more than a decade in individuals with a history of acute malaria following travel but have since lived in the complete absence of infection (Ndungu et al. 2013), suggesting that parasite-specific memory B cells can be generated and sustained without repeated exposure. Furthermore, memory B cell responses to different malaria antigens can be induced at a similar magnitude to vaccine antigenspecific responses in The Gambia, where malaria transmission is low and sporadic (Nogaro et al. 2011). Collectively, these findings suggest that variable transmission levels might affect the acquisition and maintenance of memory B cells, and lend weight to the notion that frequent clinical malaria episodes could have a detrimental effect in the generation of immunologic B cell memory. "
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