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Research Article Free access | 10.1172/JCI106817
Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
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Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
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Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
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Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
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Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
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Published February 1, 1972 - More info
Serum immunoglobulin E concentration was studied in normal children and adults, in 25 patients with isolated IgA deficiency, and in 44 patients with ataxia telangiectasia using a double antibody radioimmunoassay. The geometric mean IgE level of the normal adult population studied was 105 ng/ml, with a broad 95% interval (5-2045 ng/ml). Individuals with concentrations less than 15 ng/ml were considered to be IgE deficient. IgE deficiency, defined in this way, was observed in 7 of 73 normal adults and was not found to be associated with respiratory tract disease.
80% (35 of 44) of patients with ataxia telangiectasia (AT) were IgE deficient, 66% were IgA deficient, and 57% had combined IgE and IgA deficiencies. Although 45% of the patients with AT had respiratory tract disease, there was no correlation found between IgE deficiency or combined IgE and IgA deficiency and respiratory tract disease in these patients.
11 of 25 individuals with isolated IgA deficiency were also IgE deficient. All 11 patients with both IgA and IgE deficiency were uniformly asymptomatic. However, there was an extremely high incidence (71%) of respiratory tract disease in IgA-deficient individuals who were not IgE deficient. These data fail to support the concept of a protective role for IgE in respiratory tract immunity. The possible role of IgE in the pathogenesis of respiratory tract disease in IgA-deficient patients is discussed.