title: Complement contributes to protective immunity against reinfection by Plasmodium chabaudi chabaudi parasites.
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.
authors.affiliation: Rheumatology Section, Division of Medicine, Imperial College School of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.
authors.forename: P R
authors.initials: PR
authors.lastname: Taylor
authors.forename: E
authors.initials: E
authors.lastname: Seixas
authors.forename: M J
authors.initials: MJ
authors.lastname: Walport
authors.forename: J
authors.initials: J
authors.lastname: Langhorne
authors.forename: M
authors.initials: M
authors.lastname: Botto
mesh_terms: D000208:Acute Disease; D000818:Animals; D000913:Antibodies, Protozoan / Q000097:blood; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D003165:Complement System Proteins / Q000172:deficiency / Q000276:immunology*; D004912:Erythrocytes / Q000469:parasitology; D007371:Interferon-gamma / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D008288:Malaria / Q000276:immunology / Q000469:parasitology / Q000517:prevention & control*; D051379:Mice; D008810:Mice, Inbred C57BL; D018512:Parasitemia / Q000276:immunology / Q000469:parasitology / Q000517:prevention & control*; D016788:Plasmodium chabaudi / Q000276:immunology / Q000472:pathogenicity*; D055502:Secondary Prevention
chemical_list: D000913:Antibodies, Protozoan; D015847:Interleukin-4; D007371:Interferon-gamma; D003165:Complement System Proteins