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Front Cell Infect Microbiol. 2014 Aug 15;4:113. doi: 10.3389/fcimb.2014.00113. eCollection 2014.

Cerebral malaria: gamma-interferon redux.

Author information

1
Molecular Immunopathology Unit, School of Medical Sciences and Bosch Institute, University of Sydney Sydney, NSW, Australia.
2
Vascular Immunology Unit, School of Medical Sciences and Bosch Institute, University of Sydney Sydney, NSW, Australia.

Abstract

There are two theories that seek to explain the pathogenesis of cerebral malaria, the mechanical obstruction hypothesis and the immunopathology hypothesis. Evidence consistent with both ideas has accumulated from studies of the human disease and experimental models. Thus, some combination of these concepts seems necessary to explain the very complex pattern of changes seen in cerebral malaria. The interactions between malaria parasites, erythrocytes, the cerebral microvascular endothelium, brain parenchymal cells, platelets and microparticles need to be considered. One factor that seems able to knit together much of this complexity is the cytokine interferon-gamma (IFN-γ). In this review we consider findings from the clinical disease, in vitro models and the murine counterpart of human cerebral malaria in order to evaluate the roles played by IFN-γ in the pathogenesis of this often fatal and debilitating condition.

KEYWORDS:

CD8+T lymphocyte; blood-brain barrier; cerebral malaria; immunopathology; interferon-gamma; kynurenine pathway; microparticles; platelets

PMID:
25177551
PMCID:
PMC4133756
DOI:
10.3389/fcimb.2014.00113
[Indexed for MEDLINE]
Free PMC Article

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