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Cytoadherence and sequestration in Plasmodium falciparum: defining the ties that bind
Irwin W Sherman1, Shigetoshi Eda, Enrique Winograd
1Department of Biology, University of California, Riverside, CA 92521, USA. irwin.sherman@ucr.edu
Microbes and Infection
|August 16, 2003
Summary
Malaria parasites cause infected red blood cells to stick to blood vessels and other cells. Understanding these adhesion molecules is key to fighting Plasmodium falciparum malaria pathogenesis and survival.
Area of Science:
- Malariology
- Cellular Biology
- Immunology
Background:
- Infected erythrocytes (red blood cells) in Plasmodium falciparum malaria exhibit cytoadherence, a process crucial for parasite survival and disease development.
- Cytoadherence involves two main phenomena: sequestration (adhesion to endothelial cells) and rosetting (adhesion to uninfected erythrocytes).
Purpose of the Study:
- To critically review recent advancements in identifying molecules mediating infected erythrocyte adhesion.
- To summarize the characterized parasite-derived and host-derived molecules involved in Plasmodium falciparum sequestration and rosetting.
Main Methods:
- This review synthesizes findings from recent research studies.
- It focuses on the molecular characterization of adhesion molecules on infected erythrocytes and endothelial receptors.
Main Results:
- Key parasite-encoded adhesion molecules include PfEMP1, MESA, rifins, stevor, clag 9, and histidine-rich protein.
- Host-derived molecules on the infected erythrocyte surface include modified band 3 protein and exposed phosphatidylserine.
- Endothelial receptors involved in adhesion are thrombospondin, CD36, ICAM-1 (intercellular adhesion molecule), and chondroitin sulfate.
Conclusions:
- Understanding the molecular basis of Plasmodium falciparum adhesion is vital for developing targeted interventions.
- Characterization of these adhesion molecules provides insights into malaria pathogenesis and potential therapeutic strategies.