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Updated: Aug 13, 2026

Selection of Plasmodium falciparum Parasites for Cytoadhesion to Human Brain Endothelial Cells
Published on: January 3, 2012
The role of ICAM-1 in Plasmodium falciparum cytoadherence
Srabasti J Chakravorty1, Alister Craig
1Liverpool School of Tropical Medicine, University of Liverpool, Liverpool L3 5QA, UK. chakrasj@liverpool.ac.uk
Abstract:
Parasite sequestration at microvascular sites is a fundamental phenomenon in the manifestation of the symptoms of malaria and the progression to severe disease. Here, we review the endothelial cell-expressed intercellular adhesion molecule-1 (ICAM-1) and its role in mediating the interaction between the parasitised red blood cell (PRBC) and the vascular endothelium. We highlight the nature of the interaction between ICAM-1 and the parasite-expressed PfEMP-1 molecule at the molecular level. The review also discusses the complexity of the PRBC-endothelial cell interaction and the mechanisms that underlie parasite cytoadherence.
Insights
Malaria parasite sequestration in blood vessels involves intercellular adhesion molecule-1 (ICAM-1) on endothelial cells. This interaction with parasite proteins drives severe malaria symptoms.
Area of Science:
- Immunology
- Pathology
- Molecular Biology
Background:
- Parasite sequestration in microvasculature is key to malaria pathogenesis and severe disease.
- Endothelial cell adhesion molecules play a critical role in this process.
Purpose of the Study:
- To review the role of intercellular adhesion molecule-1 (ICAM-1) in malaria pathogenesis.
- To elucidate the molecular interactions between parasite proteins and ICAM-1.
Main Methods:
- Literature review focusing on ICAM-1 and malaria cytoadherence.
- Analysis of molecular interactions between ICAM-1 and Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1).
Main Results:
- ICAM-1 on endothelial cells mediates the binding of parasitized red blood cells (PRBCs).
- The interaction involves specific molecular recognition between ICAM-1 and PfEMP1.
- PRBC-endothelial cell interactions are complex, involving multiple cytoadherence mechanisms.
Conclusions:
- ICAM-1 is a crucial mediator of parasite sequestration in malaria.
- Understanding these molecular interactions is vital for developing strategies against severe malaria.
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Malaria

