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From The Johns Hopkins University, School of Medicine, Department of Medicine, Clinical Immunology Division at the Good Samaritan Hospital, Baltimore, Maryland 21239, the Arthritis and Clinical Immunology Units, Massachusetts General Hospital, and the Department of Medicine, Harvard Medical School, Boston, Massachusetts 02114
Abstract
Attempts were made to induce histamine release from rat mast cells exposed directly to serum from allergic patients plus specific antigen (one-stage procedure) or from mast cells initially exposed to such serum and subsequently challenged with antigen (two-stage procedure). Varying conditions of incubation, type of buffer and pH were tested; negative results were obtained. Similar attempts were made using IgE myeloma protein and rabbit antibody to IgE to induce histamine release from rat mast cells; these experiments were also unsuccessful.
IgE myeloma protein did not prepare rat skin for reverse passive cutaneous anaphylaxis mediated by anti-IgE. IgE myeloma protein which is capable, at low concentration, of inhibiting the sensitization of human basophils by IgE antibodies, failed to inhibit sensitization of rat mast cells by rat IgE antibodies both in vivo and in vitro despite its use in very high concentration. While some inhibition of the IgGa antibody-mediated release of histamine was obtained with IgE myeloma protein, large amounts of this protein were required, and some inhibition was achieved with human IgG as well, making it difficult to evaluate the inhibitory effect. The findings suggest that human IgE does not compete with rat IgE for receptors on rat peritoneal mast cells.
Footnotes
1 This work was supported by Grants AI 8270, AI 7290, AI 00423 from the National Institute of Allergy and Infectious Diseases, National Institute of Health.
2 This is Communication 66 from the O'Neill Research Laboratories of The Good Samaritan Hospital.
3 Recipient of a Research Career Development Award from the National Institute of Allergy and Infectious Diseases, National Institutes of Health.
4 Supported by Grant AI 10129 from the National Institute of Allergy and Infectious Diseases, National Institutes of Health, and grants from the Massachusetts Chapter, Arthritis Foundation and L. H. Bendit Foundation.
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