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Human Molecular Genetics, 2002, Vol. 11, No. 13 1539-1548
© 2002 Oxford University Press

Susceptibility loci for atopic dermatitis on chromosomes 3, 13, 15, 17 and 18 in a Swedish population

M. Bradley1,2,{ddagger}, C. Söderhäll1,{ddagger}, H. Luthman1,{dagger}, C.-F. Wahlgren2, I. Kockum1 and M. Nordenskjöld1,*

1Department of Molecular Medicine and 2Department of Dermatology and Venereology, Karolinska Institutet at Karolinska Hospital, SE-171 76 Stockholm, Sweden

Received February 22, 2002; Accepted April 15, 2002

Atopic dermatitis is a hereditary, pruritic, inflammatory and chronic skin disease that typically presents in early childhood and may continue or recur later. The etiology of atopic dermatitis is unknown, but several lines of evidence indicate that it is a multifactorial disorder caused by the combined influence of genetic and environmental factors, even though the relative contributions of genes and environment are not known. To identify important loci that contribute to the development of atopic dermatitis, we conducted a genome-wide linkage analysis with 367 microsatellite markers, using a non-parametric affected relative-pair method in 109 pedigrees. Three qualitative phenotypes and one semi-quantitative phenotype were studied. For the phenotype atopic dermatitis, linkage to chromosome region 3p24–22 was found. For another phenotype, atopic dermatitis combined with raised allergen-specific IgE levels, a suggestive linkage was found to chromosome region 18q21. For the semi-quantitative phenotype severity score of atopic dermatitis, suggestive linkage was found to chromosome regions 3q14, 13q14, 15q14–15 and 17q21. Identifying chromosome regions linked to susceptibility genes for atopic dermatitis provides a platform from which the search for atopic dermatitis genes can proceed.

* To whom correspondence should be addressed at: Department of Molecular Medicine, CMM 02, Karolinska Hospital, SE-171 76 Stockholm, Sweden. Fax: +46 8 51773620; Email: magnus.nordenskjold{at}cmm.ki.se

{dagger} Present address: H. Luthman, Department of Endocrinology, Wallenberg Laboratory, University Hospital MAS, SE-205 02 Malmö, Sweden.

{ddagger} The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors.


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