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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Published in | Journal of allergy and clinical immunology Vol. 99; no. 6; pp. 828 - 836 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Mosby, Inc
01.06.1997
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Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0091-6749 1097-6825 |
DOI: | 10.1016/S0091-6749(97)80018-8 |