Abstract
BackgroundThe effects of Plasmodium falciparum on B-cell homeostasis have not been well characterized. This study investigated whether an episode of acute malaria in young children results in changes in the peripheral B cell phenotype.MethodsUsing flow-cytofluorimetric analysis, the B cell phenotypes found in the peripheral blood of children aged 2–5 years were characterized during an episode of acute uncomplicated clinical malaria and four weeks post-recovery and in healthy age-matched controls.ResultsThere was a significant decrease in CD19+ B lymphocytes during acute malaria. Characterization of the CD19+ B cell subsets in the peripheral blood based on expression of IgD and CD38 revealed a significant decrease in the numbers of naive 1 CD38-IgD+ B cells while there was an increase in CD38+IgD- memory 3 B cells during acute malaria. Further analysis of the peripheral B cell phenotype also identified an expansion of transitional CD10+CD19+ B cells in children following an episode of acute malaria with up to 25% of total CD19+ B cell pool residing in this subset.ConclusionChildren experiencing an episode of acute uncomplicated clinical malaria experienced profound disturbances in B cell homeostasis.
Highlights
The effects of Plasmodium falciparum on B-cell homeostasis have not been well characterized
Dorfman et al [10] reported a diminished frequency of P. falciparumspecific memory B cells as indicated by loss of P. falciparum antibodies, and Kassa et al [11] reported a decline in total numbers of CD19+ B cells
General characteristics of the study population Twenty-five children presenting with acute clinical malaria were enrolled in this study
Summary
The effects of Plasmodium falciparum on B-cell homeostasis have not been well characterized. The primary burden of infections with P. falciparum occurs mainly in children under five years of age living in the tropical and sub-tropical areas of the world, where malaria transmission is holoendemic [2,3]. Malaria induces many pathophysiological changes including alterations in both T and B cell immunity [4]. A number of observations clearly indicate that B cells are affected by P. falciparum infection. Hypergammaglobulinaemia has been a well-described feature of Plasmodium infections [8] and persons living in malaria holoendemic regions have elevated total antibody levels [9]. Dorfman et al [10] reported a diminished frequency of P. falciparumspecific memory B cells as indicated by loss of P. falciparum antibodies, and Kassa et al [11] reported a decline in total numbers of CD19+ B cells. Polyclonal B cell activation induced by P. falciparum [9] most likely occurs through antigenic activation by the cysteine-rich interdomain region α (CIDR1α) of P. falciparum erythrocyte membrane protein 1(PfEMP1) and merozoite antigens [12]
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