Understanding Plasmodium -specific B cell dynamics during blood stage malaria infection (MPF6P.742)

• Published in: The Journal of immunology (1950) 2014-05, Vol.192 (1_Supplement), p.195-195.11
• Main Authors: Krishnamurty, Akshay, Perez-Mazliah, Damian, Pepper, Marion
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.192.Supp.195.11

Immunity to malaria is acquired gradually and comes at the expense of 1 million deaths per year. Antibodies help confer clinical immunity and longitudinal studies of those in endemic areas show that B cell mediated protection develops slowly and is maintained only with constant re-exposure. These studies, however, do not give insight to the types of B cells responding and which are most protective. Using an antigen based enrichment method we observed the dynamics of Plasmodium-specific B cells in response to blood stage Plasmodium infection against Merozoite Surface Protein 1 (MSP1), a blood stage specific protein. We find at the peak of infection the emergence of short-lived plasmablasts and as parasitemia begins to decline later arising germinal center (GC) B cells form that seed a GC-derived memory B cell population. Surprisingly, there is an emergence of GC-independent B cells, which also form a stable memory population to levels similar to that of GC-derived cells. Together these data show that in response to infection, three heterogeneous populations of Plasmodium-specific B cells emerge with two stable memory populations maintained over time. We are currently assessing the functional contributions of each of these memory populations to protective immunity. These studies represent the first glimpse of the endogenous B cell response to Plasmodium with the hopes of defining optimally protective B cell responses.