Demonstration of a common major gene with pleiotropic effects on immunoglobulin E levels and allergy

Authors

  • I. B. Borecki,

    Corresponding author
    1. Division of Biostatistics, Departments of Preventive Medicine, Washington University School of Medicine, St. Louis
    2. Psychiatry, Washington University School of Medicine, St. Louis
    • Washington University School of Medicine, Division of Biostatistics, Box 8067, 660 S. Euclid, St. Louis, MO 63110

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  • D. C. Rao,

    1. Division of Biostatistics, Departments of Preventive Medicine, Washington University School of Medicine, St. Louis
    2. Psychiatry, Washington University School of Medicine, St. Louis
    3. Genetics, Washington University School of Medicine, St. Louis
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  • J. M. Lalouel,

    1. Laboratoire d'Anthropologie Biologique, Université de Paris, Paris 7, France
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  • M. McGue,

    1. Division of Biostatistics, Departments of Preventive Medicine, Washington University School of Medicine, St. Louis
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  • J. W. Gerrard,

    1. Department of Pediatrics, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
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  • P. M. Conneally

    EditorSearch for more papers by this author

Abstract

Atopic disease is generally recognized to be familial, although specific genetic components have yet to be identified. High levels of a unique class of immunoglobulins, immunoglobulin E (IgE), have been shown to be associated with allergies. Several investigators have reported evidence indicating a recessive regulatory locus where an individual with the homozygous recessive genotype has persistently elevated levels of IgE. Willcox and Marsh [1978] have proposed a hypothesis relating IgE production and liability to become allergic. A test of this hypothesis was carried out in the present study. Bivariate segregation analysis of IgE levels and allergy was performed on 173 nuclear families, and the results indicate that an IgE regulatory locus contributes to the familial transmission of allergy. The results are further discussed in the context of the Willcox and Marsh hypothesis.

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