Hostname: page-component-848d4c4894-m9kch Total loading time: 0 Render date: 2024-05-16T19:39:17.799Z Has data issue: false hasContentIssue false

Insights into the immunopathogenesis of malaria using mouse models

Published online by Cambridge University Press:  23 March 2006

Tracey J. Lamb
Affiliation:
Division of Parasitology, National Institute for Medical Research, Mill Hill, London, NW7 1AA, UK.
Douglas E. Brown
Affiliation:
Division of Molecular Immunology, National Institute for Medical Research, Mill Hill, London, NW7 1AA, UK.
Alexandre J. Potocnik
Affiliation:
Division of Molecular Immunology, National Institute for Medical Research, Mill Hill, London, NW7 1AA, UK.
Jean Langhorne
Affiliation:
Division of Parasitology, National Institute for Medical Research, Mill Hill, London, NW7 1AA, UK.

Abstract

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.

Type
Review Article
Copyright
Cambridge University Press 2006

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)