Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 191, Issue 10, Pages 1623-1630Publisher
OXFORD UNIV PRESS INC
DOI: 10.1086/429671
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Funding
- Medical Research Council [MC_U117584248] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
- Medical Research Council [MC_U117584248] Funding Source: researchfish
- MRC [MC_U117584248] Funding Source: UKRI
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To gain insight into why antibody responses to malarial antigens tend to be short lived, we studied antigen-specific memory B cells from donors in an area where malaria is endemic. We compared antibody and memory B cell responses to tetanus toxoid with those to 3 Plasmodium falciparum candidate vaccine antigens: the C-terminal portion of merozoite surface protein 1 (MSP1(19)), apical membrane antigen 1 (AMA1), and the cysteine-rich interdomain region 1 alpha (CIDR1 alpha) of a protein from the P. falciparum erythrocyte membrane protein 1 (PfEMP1) family. These data are the first to be generated on memory B cells in children who are in the process of acquiring antimalarial immunity, and they reveal defects in B cell memory to P. falciparum antigens. Compared with the results for tetanus toxoid, more donors who were positive for antibody to AMA1 and CIDR1a were negative for memory B cells. These data imply that some exposures to malaria do not result in the establishment of stable populations of circulating antigen-specific memory B cells, suggesting possible mechanisms for the short-lived nature of many anti-malarial antibody responses.
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