High serum IgE concentrations: Association with HLA-DR and markers on chromosome 5q31 and chromosome 11q13

Background: Linkage studies mapped a locus regulating total serum IgE concentrations in a noncognate fashion to chromosome 5q31 and a locus for atopy to chromosome 11q13. In contrast, antigen-driven IgE production seems to be largely controlled by major histocompatibility complex class II genes. Obj...

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Veröffentlicht in:Journal of allergy and clinical immunology 1997-06, Vol.99 (6), p.828-836
Hauptverfasser: Ulbrecht, Matthias, Eisenhut, Tobias, Bönisch, Jürgen, Kruse, Rita, Wjst, Matthias, Heinrich, Joachim, Wichmann, Heinz-Erich, Weiss, Elisabeth H., Albert, Ekkehard D.
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Sprache:eng
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Zusammenfassung:Background: Linkage studies mapped a locus regulating total serum IgE concentrations in a noncognate fashion to chromosome 5q31 and a locus for atopy to chromosome 11q13. In contrast, antigen-driven IgE production seems to be largely controlled by major histocompatibility complex class II genes. Objective: We therefore analyzed the association between the phenotype of high IgE serum levels and six microsatellite markers on chromosomes 5q31 and 11q13, as well as HLA-DRB1, in a random sample of the adult East German population. Methods: One hundred twenty-nine persons identified as “cases” (serum IgE level>200 kU/L) and 266 control subjects (serum IgE level ≤200 kU/L) were genotyped for five 5q31 microsatellites (D5S436, D5S393, D5S210, IL-4, and IL-9) and an 11q13 microsatellite (FCERIB). Cases and controls were also typed for HLA-DRB1. Allele frequencies were compared between cases and controls by means of a twosided Fisher's exact test. Results: None of the markers was significantly associated although a weak association to the markers within the IL-9 gene and the FCERIB gene and to the HLA-DRB1 *01 allele was found when specific IgE-positive cases were compared with negative controls. Conclusions: The weak associations observed after stratification for specific IgE might point to a contribution of genes in these regions to the development of allergy.
ISSN:0091-6749
1097-6825
DOI:10.1016/S0091-6749(97)80018-8