Open Access Highly Accessed Open Badges Research

B cell analysis of ethnic groups in Mali with differential susceptibility to malaria

Silvia Portugal1, Didier Doumtabe2, Boubacar Traore2, Louis H Miller3, Marita Troye-Blomberg4, Ogobara K Doumbo2, Amagana Dolo2, Susan K Pierce1 and Peter D Crompton1*

Author Affiliations

1 Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA

2 Malaria Research and Training Centre, Department of Epidemiology of Parasitic Diseases, Faculty of Medicine, Pharmacy, and Odonto-Stomatology, University of Bamako, Bamako, Mali

3 Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA

4 Department of Immunology, Wenner-Gren Institute, Stockholm University, Stockholm, Sweden

For all author emails, please log on.

Malaria Journal 2012, 11:162  doi:10.1186/1475-2875-11-162

Published: 11 May 2012



Several studies indicate that people of the Fulani ethnic group are less susceptible to malaria compared to those of other ethnic groups living sympatrically in Africa, including the Dogon ethnic group. Although the mechanisms of this protection remain unclear, the Fulani are known to have higher levels of Plasmodium falciparum-specific antibodies of all Ig classes as compared to the Dogon. However, the proportions of B cell subsets in the Fulani and Dogon that may account for differences in the levels of Ig have not been characterized.


In this cross-sectional study, venous blood was collected from asymptomatic Fulani (n = 25) and Dogon (n = 25) adults in Mali during the malaria season, and from P. falciparum-naïve adults in the U.S. (n = 8). At the time of the blood collection, P. falciparum infection was detected by blood-smear in 16% of the Fulani and 36% of the Dogon volunteers. Thawed lymphocytes were analysed by flow cytometry to quantify B cell subsets, including immature and naïve B cells; plasma cells; and classical, activated, and atypical memory B cells (MBCs).


The overall distribution of B cell subsets was similar between Fulani and Dogon adults, although the percentage of activated MBCs was higher in the Fulani group (Fulani: 11.07% [95% CI: 9.317 – 12.82]; Dogon: 8.31% [95% CI: 6.378 – 10.23]; P = 0.016). The percentage of atypical MBCs was similar between Fulani and Dogon adults (Fulani: 28.3% [95% CI: 22.73 – 34.88]; Dogon: 29.3% [95% CI: 25.06 – 33.55], but higher than U.S. adults (U.S.: 3.0% [95% CI: -0.21 - 6.164]; P < 0.001). Plasmodium falciparum infection was associated with a higher percentage of plasma cells among Fulani (Fulani infected: 3.3% [95% CI: 1.788 – 4.744]; Fulani uninfected: 1.71% [95% CI: 1.33 – 2.08]; P = 0.011), but not Dogon adults.


These data show that the malaria-resistant Fulani have a higher percentage of activated MBCs compared to the Dogon, and that P. falciparum infection is associated with a higher percentage of plasma cells in the Fulani compared to the Dogon, findings that may account for the higher levels of P. falciparum antibodies in the Fulani.