Regulation of immunity to Plasmodium: implications from mouse models for blood stage malaria vaccine design.
Malaria, a disease caused by the protozoan parasite Plasmodium, remains a serious healthcare problem in developing countries worldwide. While the host-parasite relationship in humans has been difficult to determine, the pliability of murine malaria models has enabled valuable contributions to the understanding of the pathogenesis of disease. Although no single model reflects precisely malaria infection of the human, different models collectively provide important information on the mechanisms of protective immunity and immunopathogenesis. This review summarizes progress towards understanding the broad spectrum of immune responsiveness to the blood stages of the malaria parasite during experimental infections in mice and highlights how examination of murine malarias sheds light on the factors involved in the modulation of vaccine-potentiated immunity.
Institute of Molecular and Cellular Biology, University of Leeds, Clarendon Way, Leeds LS2 9JT, United Kingdom. a.w.taylor-robinson@leeds.ac.uk
Andrew W
AW
Taylor-Robinson
D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D004195:Disease Models, Animal; D004912:Erythrocytes / Q000276:immunology / Q000469:parasitology; D006801:Humans; D008262:Macrophage Activation / Q000276:immunology; D008288:Malaria / Q000097:blood / Q000276:immunology / Q000517:prevention & control*; D017780:Malaria Vaccines; D016779:Malaria, Cerebral / Q000276:immunology; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism; D010961:Plasmodium / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D017780:Malaria Vaccines; D009569:Nitric Oxide