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Parasite-induced B-cell apoptosis results in loss of specific protective anti-trypanosome antibody responses, and abolishment of vaccine induced protective memory responses.

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Abstract
African trypanosomes are extracellular protozoan parasites that evade the host immune response by continuous antigenic variation of their surface coat. While this ensures the escape from antibody mediated clearance, in which IgMs play a major role, we have demonstrated that in addition, trypanosomes rapidly modulate the host B-cell compartment and disable the hosts' capacity to raise a specific IgM anti-parasite response. The analysis of different B cell populations showed that during early onset of a T. brucei infection, spleen remodeling results in the rapid and permanent loss of the IgM(+) splenic marginal zone (MZ) B cell population. During infection these cells showed increased caspase activation and enzyme activity, indicating the initiation of apoptosis. When mimicking this event in vitro, by incubating trypanosome-specific IgM hybridoma cells with their corresponding parasite target, growth of the hybridoma cells was abrogated through cell-cell contact with trypanosomes. In vivo, infection-induced loss of IgM(+)MZ B cells coincided with the disappearance of protective variant-specific T-independent IgM responses, rendering mice rapidly susceptible to re-challenge with previously encountered variant antigenic type parasites. The latter suggests that during infection, no build-up of VSG-specific protective memory occurs. In addition, T. brucei infections abrogate vaccine induced protective responses to a non-related pathogen, underlining the severity of trypanosomiasis-induced B cell compartment destruction.
Keywords
BRUCEI, AFRICAN TRYPANOSOMIASIS, HSP60

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Citation

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Chicago
Magez, Stefan, V Bockstal, F Brombacher, S Black, and Magdalena Radwanska. 2010. “Parasite-induced B-cell Apoptosis Results in Loss of Specific Protective Anti-trypanosome Antibody Responses, and Abolishment of Vaccine Induced Protective Memory Responses.” In XII International Congress of Parasitology (ICOPA), 31–38. Bologna, Italy: Medimond.
APA
Magez, S., Bockstal, V., Brombacher, F., Black, S., & Radwanska, M. (2010). Parasite-induced B-cell apoptosis results in loss of specific protective anti-trypanosome antibody responses, and abolishment of vaccine induced protective memory responses. XII International congress of parasitology (ICOPA) (pp. 31–38). Presented at the 12th International congress of Parasitology (ICOPA) ; 6th Novel Approaches to the Control of Helminth Parasites of Liverstock conference, Bologna, Italy: Medimond.
Vancouver
1.
Magez S, Bockstal V, Brombacher F, Black S, Radwanska M. Parasite-induced B-cell apoptosis results in loss of specific protective anti-trypanosome antibody responses, and abolishment of vaccine induced protective memory responses. XII International congress of parasitology (ICOPA). Bologna, Italy: Medimond; 2010. p. 31–8.
MLA
Magez, Stefan et al. “Parasite-induced B-cell Apoptosis Results in Loss of Specific Protective Anti-trypanosome Antibody Responses, and Abolishment of Vaccine Induced Protective Memory Responses.” XII International Congress of Parasitology (ICOPA). Bologna, Italy: Medimond, 2010. 31–38. Print.
@inproceedings{8131866,
  abstract     = {African trypanosomes are extracellular protozoan parasites that evade the host immune response by continuous antigenic variation of their surface coat. While this ensures the escape from antibody mediated clearance, in which IgMs play a major role, we have demonstrated that in addition, trypanosomes rapidly modulate the host B-cell compartment and disable the hosts' capacity to raise a specific IgM anti-parasite response. The analysis of different B cell populations showed that during early onset of a T. brucei infection, spleen remodeling results in the rapid and permanent loss of the IgM(+) splenic marginal zone (MZ) B cell population. During infection these cells showed increased caspase activation and enzyme activity, indicating the initiation of apoptosis. When mimicking this event in vitro, by incubating trypanosome-specific IgM hybridoma cells with their corresponding parasite target, growth of the hybridoma cells was abrogated through cell-cell contact with trypanosomes. In vivo, infection-induced loss of IgM(+)MZ B cells coincided with the disappearance of protective variant-specific T-independent IgM responses, rendering mice rapidly susceptible to re-challenge with previously encountered variant antigenic type parasites. The latter suggests that during infection, no build-up of VSG-specific protective memory occurs. In addition, T. brucei infections abrogate vaccine induced protective responses to a non-related pathogen, underlining the severity of trypanosomiasis-induced B cell compartment destruction.},
  author       = {Magez, Stefan and Bockstal, V and Brombacher, F and Black, S and Radwanska, Magdalena},
  booktitle    = {XII International congress of parasitology (ICOPA)},
  isbn         = {9788875875985},
  language     = {eng},
  location     = {Melbourne, NSW, Australia},
  pages        = {31--38},
  publisher    = {Medimond},
  title        = {Parasite-induced B-cell apoptosis results in loss of specific protective anti-trypanosome antibody responses, and abolishment of vaccine induced protective memory responses.},
  year         = {2010},
}

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