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ABSTRACT MONOMERIC IgE binds tightly to the surface of mast cells and basophils without, by itself, causing any known perturbation. Interaction of the IgE with an appropriate antigen (or
experimentally with anti-IgE) causes the cells to degranulate. Little is known about the initial molecular events in IgE-mediated triggering, but there is considerable evidence that
crosslinking of the IgE molecules is a critical step (see refs 1 and 2 for discussion). The available data suggest that only limited bridging rather than an aggregation-induced extensive
redistribution of the surface IgE3,4 is required; indeed if the bridging is extensive enough to induce such gross redistribution within the time that degranulation would ordinarily be
expected, the latter is inhibited3,5. Since bridging of the IgE, and therefore of the receptor to which it is bound, seems to be a critical signal, it is important to know if the cellular
binding sites for IgE are integrated into larger functional units; the receptor molecules themselves might be multivalent, or individual receptors might be connected to each other by some
other component (Fig. 1). The experiments described here were directed towards investigating this point. We saturated cells with a mixture of two distinguishable types of rat IgE and
determined whether by redistributing one of them with specific antibody, the other would comigrate. Access through your institution Buy or subscribe This is a preview of subscription
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ACCESS OPTIONS: * Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support SIMILAR CONTENT BEING VIEWED BY OTHERS MOLECULAR MECHANISM OF IGE-MEDIATED FCΕRI
ACTIVATION Article 23 October 2024 STRUCTURAL INSIGHTS INTO THE HIGH-AFFINITY IGE RECEPTOR FCΕRI COMPLEX Article 21 August 2024 MOUSE IGG3 BINDING TO MACROPHAGE-LIKE CELLS IS PREVENTED BY
DEGLYCOSYLATION OF THE ANTIBODY OR BY ACCUTASE TREATMENT OF THE CELLS Article Open access 13 May 2021 REFERENCES * Ishizaka, K., and Ishizaka, T., _Ann. N. Y. Acad. Sci._, 190, 443–456
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INFORMATION Author notes * HENRY METZGER: Address reprint requests to: Henry Metzger, NIH, Bldg. 10, Room 9N218, Bethesda, Maryland 20014. AUTHORS AND AFFILIATIONS * Section on Chemical
Immunology, Arthritis and Rheumatism Branch, National Institute of Arthritis, Metabolism and Digestive Diseases, National Institutes of Health, Bethesda, Maryland, 20014 GUILLERMO MENDOZA
& HENRY METZGER Authors * GUILLERMO MENDOZA View author publications You can also search for this author inPubMed Google Scholar * HENRY METZGER View author publications You can also
search for this author inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE MENDOZA, G., METZGER, H. Distribution and valency of
receptor for IgE on rodent mast cells and related tumour cells. _Nature_ 264, 548–550 (1976). https://doi.org/10.1038/264548a0 Download citation * Received: 23 August 1976 * Accepted: 01
October 1976 * Published: 01 December 1976 * Issue Date: 09 December 1976 * DOI: https://doi.org/10.1038/264548a0 SHARE THIS ARTICLE Anyone you share the following link with will be able to
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