Antigen-Specific B Memory Cell Responses to Plasmodium falciparum Malaria Antigens and Schistosoma haematobium Antigens in Co-Infected Malian Children

Kirsten E Lyke,Abdoulaye Dabo,Ogobara K Doumbo,Modibo Daou,Christopher V Plowe,Marcelo B Sztein,Issa Diarra,Charles Arama,Amy Wang,Ann M Moormann

doi:10.1371/journal.pone.0037868

Abstract

Polyparasitism is common in the developing world. We have previously demonstrated that schistosomiasis-positive (SP) Malian children have age-dependent protection from malaria compared to matched schistosomiasis-negative (SN) children. Evidence of durable immunologic memory to malaria antigens is conflicting, particularly in young children and the effect of concomitant schistomiasis upon acquisition of memory is unknown. We examined antigen-specific B memory cell (MBC) frequencies (expressed as percentage of total number of IgG-secreting cells) in 84 Malian children aged 4–14 to malaria blood-stage antigens, apical membrane antigen 1 (AMA-1) and merozoite surface protein 1 (MSP-1) and to schistosomal antigens, Soluble Worm Antigenic Preparation (SWAP) and Schistosoma Egg Antigen (SEA), at a time point during the malaria transmission season and a follow-up dry season visit. We demonstrate, for the first time, MBC responses to S. haematobium antigens in Malian children with urinary egg excretion and provide evidence of seasonal acquisition of immunologic memory, age-associated differences in MBC acquisition, and correlation with circulating S. haematobium antibody. Moreover, the presence of a parasitic co-infection resulted in older children, aged 9–14 years, with underlying S. haematobium infection having significantly more MBC response to malaria antigens (AMA1 and MSP1) than their age-matched SN counterparts. We conclude that detectable MBC response can be measured against both malaria and schistosomal antigens and that the presence of S. haematobium may be associated with enhanced MBC induction in an age-specific manner.

Highlights

The acquisition of immunologic memory depends upon a rapid and specific recall response after re-exposure to an antigen
There is growing evidence that immunologic B cell memory, albeit inefficient, develops to malaria blood-stage antigens [9,10,11], but very little is known regarding the acquisition of memory to other human parasitic infections or the immunologic perturbations that one parasitic infection has upon the immune responsiveness to another infection in the host
For the first time, memory B cell response (MBC) response to S. haematobium antigens in Malian children with urinary egg excretion and provide evidence of seasonal acquisition of immunologic memory, age-associated differences in MBC acquisition, and correlation with circulating S. haematobium antibody

Summary

Introduction

The acquisition of immunologic memory depends upon a rapid and specific recall response after re-exposure to an antigen. A component of immunological memory that is central to long-term humoral immunity is the memory B cell response (MBC). MBC differentiate into antibody-secreting plasma cells that enable longterm maintenance of serum antibody levels. Long-lived plasma cells (LLPC) may reside in sequestered niches with limited space such as the bone marrow. Newly-generated plasmablasts would periodically displace these LLPC resulting in a slow decline of the compartment over time (i.e. the plasma cell niche competition model) or programming of individual plasma cells at the time of induction may determine differential lifespan (the plasma cell imprinted lifespan model) (Reviewed by Slifka) [1]. Very little is known about the acquisition of immunologic MBC to parasites. Knowledge gained regarding the acquisition of memory to parasites, are of great importance for the development of novel vaccines to both malaria and helminthes

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Conclusion