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The Molecular Genetics of Atopy

The Molecular Genetics of Atopy

Abstract

Trends in Molecular Medicine The Molecular Genetics of Atopy Asthma, rhinitis, urticaria and eczema are now easily recognised clinically. We remain largely ignorant about the mechanisms producing these symptoms. All may be produced in atopic subjects as a result of immunoglobulin E (IgE) mediated hypersensitivity. The exact cellular events and the reasons why atopic individuals exhibit only one or many of these symptoms remains unknown, as does the reason why non-atopic individuals can also develop these disorders. However, modern molecular medicine and genetics are providing new insights. The tendency to develop atopy clearly appears in successive generations of certain families. Inconsistent patterns of inheritance have been reported in family studies (1-3) and twin studies inconsistent patterns of heredity have been demonstrated for asthma. The general view was that important environmental factors influence expression and that atopy is probably independently inherited. By use of a more broad based definition of atopy than had previously been used, Cookson and colleagues cemonstrated an autosomal dominant mode of inheritance, implying a single gene defect (4). Genetic linkage analysls demonstrated that the responsible gene was sited on the long arm of chromosome 11 in an area called 1 1q13 near the centromere (
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