Expert Reviews in Molecular Medicine: http://www.expertreviews.org/
DOI: 10.1017/S1462399406010581; 24 March 2006
Tracey J. Lamb, Douglas E. Brown, Alexandre J. Potocnik and Jean Langhorne (2006) Insights into the immunopathogenesis of malaria using mouse models.
Expert Rev. Mol. Med. Vol. 8, Issue 6, DOI: 10.1017/S1462399406010581

Insights into the immunopathogenesis of malaria using mouse models

Tracey J. Lamb, Douglas E. Brown, Alexandre J. Potocnik and Jean Langhorne

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Malaria kills approximately 1–2 million people every year, mostly in sub-Saharan Africa and in Asia. These deaths are at the most severe end of a scale of pathologies affecting approximately 500 million people per year. Much of the pathogenesis of malaria is caused by inappropriate or excessive immune responses mounted by the body to eliminate malaria parasites. In this review, we examine the evidence that immunopathology is responsible for malaria disease in the context of what we have learnt from animal models of malaria. In particular, we look in detail at the processes involved in endothelial cell damage leading to syndromes such as cerebral malaria, as well as generalised systemic manifestations such as anaemia, cachexia and problems with thermoregulation of the body. We also consider malaria in light of the variation of the severity of disease observed among people, and discuss the contribution from animal models to our understanding of this variation. Finally, we discuss some of the implications of immunopathology, and of host and parasite genetic variation, for the design and implementation of anti-malarial vaccines.

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Figure 1. Plasmodium life cycle.
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Figure 2. The acute-phase reaction.
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Figure 3. Possible pathways of immunopathological organ damage inside organ vessels.
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Table 1. Mouse models of malaria.
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Table 2. Mechanisms leading to anaemia in malaria.
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Table 3. Polymorphic immune response genes associated with malarial disease.
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