Yazarlar : Bunn HF.
Yayın : Blood
Yayın Yılı : 2012
Pubmed Linki : http://www.ncbi.nlm.nih.gov/pubmed/23118217
Konu : Talasemi
Literatür İçeriği :
Abstract
The mechanisms underlying P. falciparum resistance in individuals with sickle trait have been under active investigation for over a half century. This Perspective reviews progress in solving this challenging problem including recent studies that have exploited the genomics and proteomics of the parasite. The formation of Hb S polymer in the parasitized AS red cell leads to impaired parasite growth and development along with enhanced clearance from the circulation and reduced deposition in deep post-capillary vascular beds. Enhanced generation of reactive oxygen species in sickled AS red cells is a pathogenetic feature shared by parasitized thalassemic and G6PD deficient red cells, triggering abnormal topology of the red cell plasma membrane with decreased and disordered display of PfEMP-1, a P. falciparum adhesion protein critical for endothelial adherence. A mouse model of Hb S confers host tolerance to P. berghei, through inhibition of pathogenic CD8+T cells and induction of heme oxygenase -1. An additional and apparently independent mode of protection is provided by the selective expression in AS red cells of two species of microRNA that integrate into P. falciparum mRNAs and inhibit translation and parasite growth.
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