title: Erythrocyte CR1 expression level does not correlate with a HindIII restriction fragment length polymorphism in Africans; implications for studies on malaria susceptibility.
abstract: Complement receptor 1 (CR1) expression level on erythrocytes is genetically determined, and in Caucasian populations is linked to high (H) and low (L) expression alleles identified by a HindIII restriction fragment length polymorphism (RFLP). Erythrocyte CR1 may be an important factor in determining malaria susceptibility, as low expression of CR1 reduces the rosetting of uninfected erythrocytes with Plasmodium falciparum-infected cells, a process that contributes to malaria pathogenesis. Prior to studying CR1 expression and malaria susceptibility, we have investigated whether the quantity of erythrocyte CR1 correlates with the H and L alleles in an African population. Mean erythrocyte CR1 in 149 Malian adults was 415 molecules per cell, which is comparable to Caucasian populations; however, there was no relationship between erythrocyte CR1 level and genotype for the HindIII RFLP (mean CR1 per erythrocyte HH = 414, HL = 419 and LL = 403, P > 0.1, Student's t-test). The conclusions of a previous study of erythrocyte CR1 expression level and malaria susceptibility in West Africa that was based on HindIII RFLP genotyping may therefore need to be re-evaluated.
authors.affiliation: Institute of Cell, Animal and Population Biology, University of Edinburgh, Edinburgh, UK. Alex.Rowe@ed.ac.uk
authors.forename: J A
authors.initials: JA
authors.lastname: Rowe
authors.forename: A
authors.initials: A
authors.lastname: Raza
authors.forename: D A
authors.initials: DA
authors.lastname: Diallo
authors.forename: M
authors.initials: M
authors.lastname: Baby
authors.forename: B
authors.initials: B
authors.lastname: Poudiougo
authors.forename: D
authors.initials: D
authors.lastname: Coulibaly
authors.forename: I A
authors.initials: IA
authors.lastname: Cockburn
authors.forename: J
authors.initials: J
authors.lastname: Middleton
authors.forename: K E
authors.initials: KE
authors.lastname: Lyke
authors.forename: C V
authors.initials: CV
authors.lastname: Plowe
authors.forename: O K
authors.initials: OK
authors.lastname: Doumbo
authors.forename: J M
authors.initials: JM
authors.lastname: Moulds
mesh_terms: D001741:Black or African American; D000818:Animals; D044383:Black People / Q000235:genetics; D004912:Erythrocytes / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000276:immunology; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D016778:Malaria, Falciparum / Q000235:genetics* / Q000378:metabolism; D008302:Mali; D010963:Plasmodium falciparum; D012150:Polymorphism, Restriction Fragment Length; D017463:Receptors, Complement 3b / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics*; D015265:Site-Specific DNA-Methyltransferase (Adenine-Specific) / Q000235:genetics*
chemical_list: D017463:Receptors, Complement 3b; C090528:DNA modification methylase HindIII; D015265:Site-Specific DNA-Methyltransferase (Adenine-Specific)