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dc.contributor.authorDorfman, Jeffrey R.
dc.contributor.authorBejon, Philip
dc.contributor.authorNdungu, Francis M.
dc.contributor.authorLanghorne, Jean
dc.contributor.authorKortok, Moses Mosobo
dc.contributor.authorLowe, Brett S.
dc.contributor.authorMwangi, Tabitha
dc.contributor.authorWilliams, Thomas N.
dc.contributor.authorMarsh, Kevin
dc.date.accessioned2013-11-06T08:52:06Z
dc.date.available2013-11-06T08:52:06Z
dc.date.issued2005-05
dc.identifier.urihttp://hdl.handle.net/123456789/593
dc.description.abstractTo gain insight into why antibody responses to malarial antigens tend to be short lived, we studied antigenspecific 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 Cterminal portion of merozoite surface protein 1 (MSP119), apical membrane antigen 1 (AMA1), and the cysteinerich interdomain region 1a (CIDR1a) 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.en_US
dc.language.isoenen_US
dc.publisherJournal of Infectious Diseasesen_US
dc.titleB Cell Memory to 3 Plasmodium falciparum Blood-Stage Antigens in a Malaria-Endemic Areaen_US
dc.typeArticleen_US


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