Major quantitative trait locus for eosinophil count is located on chromosome 2q - 25/08/11
, Gu Zhu, MD a, David L. Duffy, MBBS, PhD a, Grant W. Montgomery, PhD a, Ian H. Frazer, MD c, Nicholas G. Martin, PhD a
Reprint requests: David M. Evans, PhD, Wellcome Trust Centre for Human Genetics, Roosevelt Drive, Oxford, OX3 7BN, United Kingdom.Brisbane, Australia, and Oxford, United Kingdom
Résumé |
Background |
Eosinophils are granulocytic white blood cells implicated in asthma and atopic disease. The degree of eosinophilia in the blood of patients with asthma correlates with the severity of asthmatic symptoms. Quantitative trait loci (QTL) linkage analysis of eosinophil count may be a more powerful strategy of mapping genes involved in asthma than linkage analysis using affected relative pairs.
Objective |
To identify QTLs responsible for variation in eosinophil count in adolescent twins.
Methods |
We measured eosinophil count longitudinally in 738 pairs of twins at 12, 14, and 16 years of age. We typed 757 highly polymorphic microsatellite markers at an average spacing of 
5 centimorgans across the genome. We then used multipoint variance components linkage analysis to test for linkage between marker loci and eosinophil concentrations at each age across the genome.
Results |
We found highly significant linkage on chromosome 2q33 in 12-year-old twins (logarithm of the odds=4.6; P=.000002) and suggestive evidence of linkage in the same region in 14-year-olds (logarithm of the odds=1.0; P=.016). We also found suggestive evidence of linkage at other areas of the genome, including regions on chromosomes 2, 3, 4, 8, 9, 11, 12, 17, 20, and 22.
Conclusion |
A QTL for eosinophil count is present on chromosome 2q33. This QTL might represent a gene involved in asthma pathophysiology.
Le texte complet de cet article est disponible en PDF.Key words : Eosinophils, asthma, genetics, linkage, QTL, twins
Abbreviations used : cM, IBD, LOD, QTL
Plan
| Funding source: collection of phenotypes and DNA samples was supported by grants from the Queensland Cancer Fund, the Australian National Health and Medical Research Council (950998, 981339, and 241944) and the US National Cancer Institute (CA88363) to Dr Nick Hayward. The genome scans were supported by the Australian National Health and Medical Research Council's Program in Medical Genomics and funding from the Center for Inherited Disease Research (Director, Dr Jerry Roberts) at Johns Hopkins University to Dr Jeff Trent. |
Vol 114 - N° 4
P. 826-830 - octobre 2004 Retour au numéro
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