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, Stefan en_ZA
dc.contributor.author Schwegmann, Anita en_ZA
dc.contributor.author Atkinson, Robert en_ZA
dc.contributor.author Claes, Filip en_ZA
dc.contributor.author Drennan, Michael en_ZA
dc.contributor.author De Baetselier, Patrick en_ZA
dc.contributor.author Brombacher, Frank en_ZA
dc.date.accessioned 2015-11-23T12:35:22Z
dc.date.available 2015-11-23T12:35:22Z
dc.date.issued 2008 en_ZA
dc.identifier.citation 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 Pathog, 4(8), e1000122. doi:10.1371/journal.ppat.1000122 en_ZA
dc.identifier.uri http://hdl.handle.net/11427/15326
dc.identifier.uri http://dx.doi.org/10.1371/journal.ppat.1000122
dc.description.abstract Author Summary African trypanosomiasis is a disease caused by different species of extracellular flagellated protozoan trypanosome parasites. Trypanosomes have developed a mechanism of regular antigenic variation of their variant-specific surface glycoprotein (VSG) coat which allows chronic infection. Replacement of this coat occurs at rapid regular time intervals, allowing the parasite to escape from an effective host antibody responses. So far, primary T-cell independent antibody responses have been described to constitute the main host defense mechanism, relying largely on IgM antibody induction. Using genetically engineered B lymphocyte- or IgM-deficient mouse strains, we show that lack of B-cells or IgM did not prevent infection-associated anemia. More importantly, we show that in the absence of IgM, parasitemia was controlled almost as well as in wild-type mice, with only slightly increased mortality. In addition, we show in vivo that antigenic variation is not affected by the lack of IgM. en_ZA
dc.language.iso eng en_ZA
dc.publisher Public Library of Science en_ZA
dc.rights This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. en_ZA
dc.rights.uri http://creativecommons.org/licenses/by/4.0 en_ZA
dc.source PLoS One en_ZA
dc.source.uri http://journals.plos.org/plospathogens en_ZA
dc.subject.other Parasitic diseases en_ZA
dc.subject.other Antibodies en_ZA
dc.subject.other B cells en_ZA
dc.subject.other Host-pathogen interactions en_ZA
dc.subject.other Parasitemia en_ZA
dc.subject.other Anemia en_ZA
dc.subject.other Trypanosoma brucei gambiense en_ZA
dc.subject.other Trypanosomiasis en_ZA
dc.title The role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice en_ZA
dc.type Journal Article en_ZA
dc.rights.holder © 2008 Magez et al en_ZA
uct.type.publication Research en_ZA
uct.type.resource Article en_ZA
dc.publisher.institution University of Cape Town
dc.publisher.faculty Faculty of Health Sciences en_ZA
dc.publisher.department Division of Immunology en_ZA
uct.type.filetype Text
uct.type.filetype Image
dc.identifier.apacitation 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. <i>PLoS One</i>, http://hdl.handle.net/11427/15326 en_ZA
dc.identifier.chicagocitation Magez, Stefan, Anita Schwegmann, Robert Atkinson, Filip Claes, Michael Drennan, Patrick De Baetselier, and Frank Brombacher "The role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice." <i>PLoS One</i> (2008) http://hdl.handle.net/11427/15326 en_ZA
dc.identifier.vancouvercitation 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 One. 2008; http://hdl.handle.net/11427/15326. en_ZA
dc.identifier.ris TY - Journal Article AU - Magez, Stefan AU - Schwegmann, Anita AU - Atkinson, Robert AU - Claes, Filip AU - Drennan, Michael AU - De Baetselier, Patrick AU - Brombacher, Frank AB - Author Summary African trypanosomiasis is a disease caused by different species of extracellular flagellated protozoan trypanosome parasites. Trypanosomes have developed a mechanism of regular antigenic variation of their variant-specific surface glycoprotein (VSG) coat which allows chronic infection. Replacement of this coat occurs at rapid regular time intervals, allowing the parasite to escape from an effective host antibody responses. So far, primary T-cell independent antibody responses have been described to constitute the main host defense mechanism, relying largely on IgM antibody induction. Using genetically engineered B lymphocyte- or IgM-deficient mouse strains, we show that lack of B-cells or IgM did not prevent infection-associated anemia. More importantly, we show that in the absence of IgM, parasitemia was controlled almost as well as in wild-type mice, with only slightly increased mortality. In addition, we show in vivo that antigenic variation is not affected by the lack of IgM. DA - 2008 DB - OpenUCT DO - 10.1371/journal.ppat.1000122 DP - University of Cape Town J1 - PLoS One LK - https://open.uct.ac.za PB - University of Cape Town PY - 2008 T1 - The role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice TI - The role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice UR - http://hdl.handle.net/11427/15326 ER - en_ZA


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This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Except where otherwise noted, this item's license is described as This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.