Association study of the chromosomal region containing the FCER2 gene suggests it has a regulatory role in atopic disorders

Citation
T. Laitinen et al., Association study of the chromosomal region containing the FCER2 gene suggests it has a regulatory role in atopic disorders, AM J R CRIT, 161(3), 2000, pp. 700-706
Citations number
31
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
ISSN journal
1073-449X → ACNP
Volume
161
Issue
3
Year of publication
2000
Pages
700 - 706
Database
ISI
SICI code
1073-449X(200003)161:3<700:ASOTCR>2.0.ZU;2-N
Abstract
On the basis of studies with animal models, the gene for the low-affinity r eceptor Per immunoglobulin E (IgE) (FCER2, CD23) has been implicated as a c andidate for IgE-mediated allergic diseases and bronchial hyperreactivity, or related traits. Given evidence for genetic complexity in atopic disorder s, we sought to study two European subpopulations, Finnish and Catalonian. We studied three phenotypic markers: (1) total serum IgE level; (2) asthma; and (3) specific IgE level for a mixture of the most common aeroallergens in Finland. Altogether, eight polymorphic markers spanning a region of 10 c M around the FCER2 gene on chromosome 19p13 were analyzed in 124 families. The physical order of the markers and the location of the FCER2 gene were c onfirmed by using radiation hybrids. The allele and haplotype association s tudy showed a suggestive haplotype association (signficance of p less than or equal to 0.03 based on a permutation test) for a high serum IgE response . In a subset of chromosomes segregating with asthma in families with two o r more affected members, a single haplotype was found to be highly enriched (p = 8.3 x 10(-6)). However, sequence polymorphisms, which would verify st ructural differences in the FCER2 gene, were not detected in the coding reg ion of: the receptor. Our results suggest that chromosome 19p13 might harbo r a genetic determinant of IgE-related traits. Studies in other population samples are needed to verify this finding.