The B cell response to Plasmodium chabaudi chabaudi malaria in the mouse model

Achtman, Ariel H. (2004). The B cell response to Plasmodium chabaudi chabaudi malaria in the mouse model. PhD thesis The Open University.



This thesis characterises the B cell response of C57BL/6 mice after infection with Plasmodium chabaudi chabaudi (AS) with regard to plasma cell longevity, B cell memory and the specific response to part of the merozoite surface protein-1 (MSP-1 21), an antigen involved in protection against malaria. Infected spleens showed massive but reversible disruption of the white pulp architecture around the peak of infection. Nevertheless, strong plasma cell and germinal centre responses were detected along with atypical plasma cell location and apparent involvement of marginal zone B cells. The MSP-1 21-specific B cell response to primary infection did not display any obvious abnormalities at the cellular level. The longevity of protection was assessed in the presence and absence of parasites. P. c. chabaudi parasites persisted for 2-3 months after infection. A single infection mediated protection in form of reduced parasitaemias for up to 9 months. When mice were reinfected after 2.5 months but not later, the presence of parasites from the primary infection led to an additional reduction. This can be attributed to cooperation between effector and memory cells.

MSP-1 21-specific IgG levels were measured in primary and secondary infections and during the intervening period. Plasma levels of IgG against MSP-1 21 and crude malarial extract drop significantly between 1 and 2. 5 months post infection and then remain constant, suggesting that Plasmodium-specific plasma IgG levels are maintained by long-lived plasma cells independent of parasite presence or absence after day 30. However, MSP-1 21-specific memory B cell generation, maintenance or reactivation appears to be reduced in the presence of parasites albeit with increased affinity maturation. Primary and secondary antibody responses to MSP-1 21 develop more slowly than antibody responses observed in other infections, suggesting that despite the strong B cell response during primary infection with malaria, there is an impairment of the B cell response at some level.

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