Abstract |
It is proposed that the surface ligands of Plasmodium falciparum infected HbAS erythrocytes, not like infected HbAA erythrocytes, are altered due to the sickling that soon takes place once a HbAS erythrocyte gets infected with P. falciparum parasite. This alteration modulates cytoadherence and/or binding of the sickled erythrocytes to the peripheral blood mononuclear cells (PBMCs). Both cytoadherence and binding to PBMCs are responsible for the pathogenesis of malaria. Therefore, subjects of the HbAS genotype experience mild symptoms of malaria. The hypothesis could be tested in vitro by comparing the binding of P. falciparum infected HbAS and HbAA erythrocytes to platelet-endothelial cell adhesion molecule-1 (CD31) and by comparing the levels of tumor necrosis factor (TNF) and interferon gamma (IFN-gamma) following in vitro stimulation of PBMCs by HbAS and HbAA infected erythrocytes.
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Authors | N H Abdulhadi |
Journal | Medical hypotheses
(Med Hypotheses)
Vol. 60
Issue 6
Pg. 912-4
(Jun 2003)
ISSN: 0306-9877 [Print] United States |
PMID | 12699725
(Publication Type: Journal Article)
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Chemical References |
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Topics |
- Cell Adhesion
(immunology)
- Cytokines
(metabolism)
- Erythrocyte Aggregation
(immunology)
- Humans
- Immunity, Innate
(immunology)
- Malaria, Falciparum
(classification, immunology, metabolism)
- Severity of Illness Index
- Sickle Cell Trait
(immunology, metabolism)
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