Annals of Saudi Medicine
Publication of the King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia
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ORIGINAL ARTICLE
Year : 2010  |  Volume : 30  |  Issue : 2  |  Page : 115-122

Linkage and haplotype analysis for chemokine receptors clustered on chromosome 3p21.3 and transmitted in family pedigrees with asthma and atopy


1 Department of Child Health, Royal Aberdeen Children's Hospital, University of Aberdeen, Medical School, Westburn Road, Aberdeen, Scotland, United Kingdom,
2 Department of Hematology and Immunology, College of Medicine, Umm Al-Qura University, Makkah, Saudi Arabia,

Correspondence Address:
Saleh A Al-Abdulhadi
Medical Molecular Genetic and Genetic Counselling, Molecular Genetic Section and Counselling Clinic, Department of Pathology and Laboratory Medicine, Saad Specialist Hospital, Al-khubar, Saudi Arabia

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DOI: 10.4103/0256-4947.60516

PMID: 20220260



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Background and Objectives : Genomic scan analyses have suggested that the chemokine receptor cluster (CCR2, CCR3, CCR5 <300 kb span) on the short arm of chromosome 3 may contribute to susceptibility to HIV-1 infection and to the expression of a number of inflammatory diseases. Two single nucleotide polymorphisms (SNP) and a deletion in these chemokine receptors have also been found in case-control studies to be associated with susceptibility for asthma and related phenotypes. We extended these case-control studies by establishing whether these polymorphisms were in linkage and linkage disequilibrium with asthma and related phenotypes using linkage and haplotype analyses. Methods : We genotyped 154 nuclear families identified through two child probands with physician-diagnosed asthma (453 unrelated individuals) including 303 unrelated parents and 150 unrelated children. Atopy was defined as a positive skin prick test (SPT 3 mm) to a panel of common inhaled allergens. Results : From a panel of ten known SNPs, only three polymorphisms: -G190A in CCR2, -T51C in CCR3, and a 32 bp deletion in CCR5 were found to occur at clinically relevant frequencies. All 154 families were used for haplotype analysis but only 12 nuclear families were eligible for linkage analysis. Both analyses confirmed that the mutations were in linkage with asthma, but not with atopy. Conclusion : The chemokine receptor genes on 3p21.3 are significantly plausible candidate genes that can influence the expression of asthma. The previous association of the CCR5∆32 deletion with protection from childhood asthma appears to be explained by linkage disequilibrium with the -G190A mutation in the CCR2 receptor gene.


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