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Research Article Free access | 10.1172/JCI109514
Department of Immunopathology, Scripps Clinic and Research Foundation, La Jolla, California 92037
Department of Clinical Research, Scripps Clinic and Research Foundation, La Jolla, California 92037
Department of Pediatrics, University of California at San Diego, La Jolla, California 92093
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Department of Immunopathology, Scripps Clinic and Research Foundation, La Jolla, California 92037
Department of Clinical Research, Scripps Clinic and Research Foundation, La Jolla, California 92037
Department of Pediatrics, University of California at San Diego, La Jolla, California 92093
Find articles by O'Connor, R. in: JCI | PubMed | Google Scholar
Department of Immunopathology, Scripps Clinic and Research Foundation, La Jolla, California 92037
Department of Clinical Research, Scripps Clinic and Research Foundation, La Jolla, California 92037
Department of Pediatrics, University of California at San Diego, La Jolla, California 92093
Find articles by Simon, R. in: JCI | PubMed | Google Scholar
Department of Immunopathology, Scripps Clinic and Research Foundation, La Jolla, California 92037
Department of Clinical Research, Scripps Clinic and Research Foundation, La Jolla, California 92037
Department of Pediatrics, University of California at San Diego, La Jolla, California 92093
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Published September 1, 1979 - More info
Lymphocytes from normal nonallergic donors and patients with atopic disorders were analyzed for subpopulations bearing Fc receptors for immunoglobulin (Ig)E (Fcε) and IgG (Fcγ), surface IgM (sIgM) and IgD (sIgD), and for T cells forming spontaneous rosettes with sheep erythrocytes (E). The patients were divided into three groups according to serum IgE concentrations and systemic corticosteroid treatment. Group I consisted of 12 atopic patients with either normal or moderately increased IgE levels up to 4,000 U/ml. Four patients of group II and three of group III had 10,500-31,000 U/ml and severe atopic dermatitis. Patients of group III, but not I and II, were receiving corticosteroids systemically. The percentage (mean ±SD) and total number of Fcε+ lymphocytes were 1.2±0.5%, 41±24/mm3 in 12 normals; 1.6±0.9%, 59±43/mm3 in patients of group I: 7.0±2.0%, 187±67/mm3 in group II; and 0.3±0.1%, 13±5/mm3 in patients of group III. The increase in group II and decrease in group III of Fcε+ cells were statistically significantly different from the normal persons and patients of group I. In contrast, the patients did not differ significantly from the donors in sIgM+, sIgD+, Fcγ+, and E+ cell populations. As shown by depletion of sIg+ cells in four patients with atopic disorders, the great majority of the Fcε+ lymphocytes were B cells. However, two patients with elevated Fcε+ cell numbers had small numbers of mixed E- and Fcε-rosetting cells, presumably T cells. Two patients of group II were examined during an acute herpes simplex infection. Both showed an ≅80% decrease of Fcε+ cells at that time. No apparent correlation between numbers of Fcε+ cells and IgE level existed in patients of group I. Injection of an IgE myeloma protein into two monkeys did not significantly change their percentages of Fcε+ lymphocytes.
The data indicate that Fcε+ lymphocytes are increased in patients with markedly elevated serum IgE and severe atopic disease, suggesting that these cells may be involved in the regulation and(or) synthesis of IgE antibody formation.