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Research Article Free access | 10.1172/JCI106890
Department of Medicine, University of New Mexico School of Medicine, Albuquerque, New Mexico 87106
Department of Medicine, William Beaumont Army Hospital, El Paso, Texas 79920
Department of Medicine, Lovelace Clinic, Albuquerque, New Mexico 87108
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Department of Medicine, University of New Mexico School of Medicine, Albuquerque, New Mexico 87106
Department of Medicine, William Beaumont Army Hospital, El Paso, Texas 79920
Department of Medicine, Lovelace Clinic, Albuquerque, New Mexico 87108
Find articles by Griffiths, R. in: JCI | PubMed | Google Scholar
Department of Medicine, University of New Mexico School of Medicine, Albuquerque, New Mexico 87106
Department of Medicine, William Beaumont Army Hospital, El Paso, Texas 79920
Department of Medicine, Lovelace Clinic, Albuquerque, New Mexico 87108
Find articles by Emmons, J. in: JCI | PubMed | Google Scholar
Department of Medicine, University of New Mexico School of Medicine, Albuquerque, New Mexico 87106
Department of Medicine, William Beaumont Army Hospital, El Paso, Texas 79920
Department of Medicine, Lovelace Clinic, Albuquerque, New Mexico 87108
Find articles by Field, R. in: JCI | PubMed | Google Scholar
Published April 1, 1972 - More info
Human sera have been examined for antibodies with specific reactivity for γE using the tanned cell hemagglutination test. Cells tanned with three different γE myeloma proteins provided a reproducible test system. Inhibition of agglutination reactions by γE proteins, but not by γG, γA, γM, or γD confirmed the specificity of these reactions. 8.5% of 304 serial serum samples obtained from miscellaneous hospitalized patients showed clear-cut anti-γ-globulins with specificity for γE. In most of these instances no definite clinical history of concomitant allergic disorders could be obtained. 53% of 73 patients with well-established allergic disorders (hay fever, extrinsic asthma) showed serum anti-γ-globulins with reactivity for γE. Some patients studied before and after desensitization to Bermuda grass allergen showed an increase in titer or a conversion from negative to positive reactions for anti-γE antibodies following several month courses of progressive desensitization. Gradient and gel filtration studies indicated that anti-γE globulins were 19S γM in all instances. No clear correlation was noted between quantitative serum γE levels and titer of anti-γE antibodies.
19S serum fractions with anti-γE antibody activity did not release histamine from normal human peripheral blood leukocytes, whereas specific rabbit anti-γE antisera consistently induced leukocytic histamine release. Moreover, macroglobulin fractions with anti-γE activity did not block allergen-specific leukocyte histamine release induced by in vitro leukocyte challenge with allergens such as Bermuda grass and leukocytes from allergic donors. In some instances 19S human serum fractions with anti-γE activity appeared to potentiate histamine release when incubated concomitantly with specific allergen and leukocytes from allergic individuals.