Complement contributes to protective immunity against reinfection by Plasmodium chabaudi chabaudi parasites |
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| Authors: | Taylor P R Seixas E Walport M J Langhorne J Botto M |
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| Affiliation: | Rheumatology Section, Division of Medicine, Imperial College School of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom. |
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| Abstract: | We have studied the impact of deficiency of the complement system on the progression and control of the erythrocyte stages of the malarial parasite Plasmodium chabaudi chabaudi. C1q-deficient mice and factor B- and C2-deficient mice, deficient in the classical complement pathway and in both the alternative and classical complement activation pathways, respectively, exhibited only a slight delay in the resolution of the acute phase of parasitemia. Complement-deficient mice showed a transiently elevated level of gamma interferon (IFN-gamma) in the plasma at the time of the acute parasitemia compared with that of wild-type mice. Although there was a trend for increased precursor frequencies in CD4(+) T cells from C1q-deficient mice producing IFN-gamma in response to malarial antigens in vitro, intracellular cytokine staining of spleen cells ex vivo showed no difference in the numbers of IFN-gamma(+) splenic CD4(+) and CD8(+) cells. In contrast, C1q-deficient animals were significantly more susceptible to a second challenge with the same parasite. C1q-deficient animals showed a reduced level of anti-malarial immunoglobulin G2a (IgG2a) antibody 100 days after primary infection. However, following a significantly higher parasitemia, C1q-deficient mice had increased levels of IgM and IgG2a anti-malarial antibodies. In summary, this study indicates that while complement plays only a minor role in the control of the acute phase of parasitemia of a primary infection, it does contribute to parasite control in reinfection. |
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