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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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dc.contributor.author Magez, S.
dc.contributor.author Schwegmann, A.
dc.contributor.author Atkinson, R.
dc.contributor.author Claes, F.
dc.contributor.author Drennan, M.
dc.contributor.author De Baetselier, P.
dc.contributor.author Brombacher, F.
dc.date.accessioned 2008-10-28T13:50:56Z
dc.date.available 2008-10-28T13:50:56Z
dc.date.issued 2008
dc.identifier.issn 1553-7366
dc.identifier.doi http://dx.doi.org/10.1371/journal.ppat.1000122
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.identifier.uri http://hdl.handle.net/10390/2403
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.identifier.pmid http://www.ncbi.nlm.nih.gov/pubmed/18688274
dc.citation.jabbreviation PLoS Pathog en_US


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