Complement Contributes to Protective Immunity against Reinfection byPlasmodium chabaudi chabaudiParasites
Open Access
- 1 June 2001
- journal article
- Published by American Society for Microbiology in Infection and Immunity
- Vol. 69 (6), 3853-3859
- https://doi.org/10.1128/iai.69.6.3853-3859.2001
Abstract
We have studied the impact of deficiency of the complement system on the progression and control of the erythrocyte stages of the malarial parasitePlasmodium 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-γ) 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-γ in response to malarial antigens in vitro, intracellular cytokine staining of spleen cells ex vivo showed no difference in the numbers of IFN-γ+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.Keywords
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