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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
biochemistry, genetics and molecular biology
The role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice
PLoS Pathogens, Volume 4, No. 8, Article e1000122, Year 2008
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Description
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 (μMT) and IgM-deficient (IgM -/-) 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 μMT and IgM -/- 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 μMT mice as well as in IgM-/- 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. © 2008 Magez et al.
Authors & Co-Authors
Magez, Stefan
South Africa, Cape Town
University of Cape Town
Italy, Trieste
International Centre for Genetic Engineering and Biotechnology
Belgium, Ghent
Vlaams Instituut Voor Biotechnologie
Belgium, Brussels
Vrije Universiteit Brussel
Schwegmann, Anita
South Africa, Cape Town
University of Cape Town
Italy, Trieste
International Centre for Genetic Engineering and Biotechnology
Atkinson, Robert A.
South Africa, Cape Town
University of Cape Town
Italy, Trieste
International Centre for Genetic Engineering and Biotechnology
Claes, Filip
Belgium, Antwerpen
Prins Leopold Instituut Voor Tropische Geneeskunde
Drennan, Michael B.
South Africa, Cape Town
University of Cape Town
Italy, Trieste
International Centre for Genetic Engineering and Biotechnology
Belgium, Ghent
Vlaams Instituut Voor Biotechnologie
de Baetseĺier, Patrick C.
Belgium, Ghent
Vlaams Instituut Voor Biotechnologie
Belgium, Brussels
Vrije Universiteit Brussel
Brombacher, Frank
South Africa, Cape Town
University of Cape Town
Italy, Trieste
International Centre for Genetic Engineering and Biotechnology
Statistics
Citations: 87
Authors: 7
Affiliations: 5
Identifiers
Doi:
10.1371/journal.ppat.1000122
ISSN:
15537366
e-ISSN:
15537374