Plasmodium yoelii Can Ablate Vaccine-Induced Long-Term Protection in Mice

Malaria is a serious cause of morbidity and mortality for people living in endemic areas, but unlike many other infections, individuals exposed to the parasite do not rapidly become resistant to subsequent infections. High titers of Ab against the 19-kDa C-terminal fragment of the merozoite surface...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2005-08, Vol.175 (4), p.2510-2516
Main Authors: Wykes, Michelle N, Zhou, Yong-Hong, Liu, Xue Q, Good, Michael F
Format: Article
Language:English
Subjects:
Animals
Apoptosis - immunology
B-Lymphocyte Subsets - immunology
B-Lymphocyte Subsets - parasitology
B-Lymphocyte Subsets - transplantation
Bystander Effect - immunology
Cell Survival - immunology
Immunologic Memory
Malaria - immunology
Malaria - parasitology
Malaria - pathology
Malaria - prevention & control
Malaria Vaccines - administration & dosage
Malaria Vaccines - antagonists & inhibitors
Malaria Vaccines - immunology
Merozoite Surface Protein 1 - administration & dosage
Merozoite Surface Protein 1 - immunology
Mice
Mice, Inbred BALB C
Mice, SCID
Plasma Cells - cytology
Plasma Cells - immunology
Plasmodium yoelii - immunology
Time Factors
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Summary:Malaria is a serious cause of morbidity and mortality for people living in endemic areas, but unlike many other infections, individuals exposed to the parasite do not rapidly become resistant to subsequent infections. High titers of Ab against the 19-kDa C-terminal fragment of the merozoite surface protein-1 can mediate complete protection in model systems; however, previous studies had not determined whether this vaccine generated long-term protection. In this study, we report that functional memory cells generated by merozoite surface protein-1, per se, do not offer any protection. This is because the parasite induces deletion of vaccine-specific memory B cells as well as long-lived plasma cells including those specific for bystander immune responses. Our study demonstrates a novel mechanism by which Plasmodium ablates immunological memory of vaccines, which would leave the host immuno-compromised.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.175.4.2510