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

(2008) PLOS PATHOGENS. 4(8).
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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 (mu MT) 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 mu MT 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 mu MT 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.
Keywords
NECROSIS-FACTOR-ALPHA, BLOOD-STREAM FORMS, AFRICAN TRYPANOSOMIASIS, RHODESIENSE INFECTION, ANTIGENIC VARIATION, EXPRESSION SITE, RESPONSES, CONGOLENSE, PATHOGENESIS, GENE

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Citation

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Chicago
Magez, Stefan, Anita Schwegmann, Robert Atkinson, Filip Claes, Michael Drennan, Patrick De Baetselier, and Frank Brombacher. 2008. “The Role of B-cells and IgM Antibodies in Parasitemia, Anemia, and VSG Switching in Trypanosoma Brucei-infected Mice.” Plos Pathogens 4 (8).
APA
Magez, S., Schwegmann, A., Atkinson, R., Claes, F., Drennan, M., De Baetselier, P., & Brombacher, F. (2008). The role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice. PLOS PATHOGENS, 4(8).
Vancouver
1.
Magez S, Schwegmann A, Atkinson R, Claes F, Drennan M, De Baetselier P, et al. The role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice. PLOS PATHOGENS. 2008;4(8).
MLA
Magez, Stefan et al. “The Role of B-cells and IgM Antibodies in Parasitemia, Anemia, and VSG Switching in Trypanosoma Brucei-infected Mice.” PLOS PATHOGENS 4.8 (2008): n. pag. Print.
@article{8614899,
  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 (mu MT) 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 mu MT 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 mu MT 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.},
  articleno    = {e1000122},
  author       = {Magez, Stefan and Schwegmann, Anita and Atkinson, Robert and Claes, Filip and Drennan, Michael and De Baetselier, Patrick and Brombacher, Frank},
  issn         = {1553-7366},
  journal      = {PLOS PATHOGENS},
  keywords     = {NECROSIS-FACTOR-ALPHA,BLOOD-STREAM FORMS,AFRICAN TRYPANOSOMIASIS,RHODESIENSE INFECTION,ANTIGENIC VARIATION,EXPRESSION SITE,RESPONSES,CONGOLENSE,PATHOGENESIS,GENE},
  language     = {eng},
  number       = {8},
  pages        = {12},
  title        = {The role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice},
  url          = {http://dx.doi.org/10.1371/journal.ppat.1000122},
  volume       = {4},
  year         = {2008},
}

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