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The role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice

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Show simple item record Magez, S. Schwegmann, A. Atkinson, R. Claes, F. Drennan, M. De Baetselier, P. Brombacher, F. 2008-10-28T13:50:56Z 2008-10-28T13:50:56Z 2008
dc.identifier.issn 1553-7366
dc.identifier.other ITG-P4A
dc.identifier.other PARAS
dc.identifier.other U-SEROL
dc.identifier.other JIF
dc.identifier.other ELECTRONIC
dc.identifier.other DOI
dc.identifier.other ABSTRACT
dc.identifier.other UPD7
dc.identifier.other FTA
dc.description.abstract African trypanosomes are extracellular parasitic protozoa, predominantly transmitted by the bite of the haematophagic tsetse fly. The main mechanism considered to mediate parasitemia control in a mammalian host is the continuous interaction between antibodies and the parasite surface, covered by variant-specific surface glycoproteins. Early experimental studies have shown that B-cell responses can be strongly protective but are limited by their VSG-specificity. We have used B-cell (mMT) and IgM-deficient (IgM2/2) mice to investigate the role of B-cells and IgM antibodies in parasitemia control and the in vivo induction of trypanosomiasis-associated anemia. These infection studies revealed that that the initial setting of peak levels of parasitemia in Trypanosoma brucei–infected mMT and IgM2/2 mice occurred independent of the presence of B-cells. However, B-cells helped to periodically reduce circulating parasites levels and were required for long term survival, while IgM antibodies played only a limited role in this process. Infection-associated anemia, hypothesized to be mediated by B-cell responses, was induced during infection in mMT mice as well as in IgM2/2 mice, and as such occurred independently from the infection-induced host antibody response. Antigenic variation, the main immune evasion mechanism of African trypanosomes, occurred independently from host antibody responses against the parasite’s ever-changing antigenic glycoprotein coat. Collectively, these results demonstrated that in murine experimental T. brucei trypanosomiasis, B-cells were crucial for periodic peak parasitemia clearance, whereas parasite-induced IgM antibodies played only a limited role in the outcome of the infection. en_US
dc.language English en_US
dc.subject Protozoology en_US
dc.subject Trypanosoma brucei en_US
dc.subject Murine en_US
dc.subject Parasitemia en_US
dc.subject Anemia en_US
dc.subject B-cells en_US
dc.subject IgM antibodies en_US
dc.subject Role en_US
dc.subject Surface glycoproteins en_US
dc.subject Antigenic variation en_US
dc.title The role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice en_US
dc.type Article-E en_US
dc.citation.issue 8 en_US
dc.citation.jtitle PLoS Pathogens en_US
dc.citation.volume 4 en_US
dc.citation.pages e1000122 en_US
dc.citation.jabbreviation PLoS Pathog en_US

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