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Interaction of IgE with Rat Basophilic Leukemia Cells

IV. Antibody-Induced Redistribution of IgE Receptors

From the Arthritis and Rheumatism Branch, National Institute of Arthritis, Metabolism and Digestive Diseases, National Institutes of Health, Bethesda, Maryland 20014

Abstract

Rat leukemic basophils with surface-bound IgE were reacted with fluoresceinated anti-IgE. The results were qualitatively similar to those obtained in analogous studies with lymphocytes, normal human basophils, and other cells: local aggregation (patch formation) was only moderately temperature-dependent and was uninhibited by NaN₃. Polar cap formation was significantly more sensitive to temperature and was completely inhibited by 0.01 to 0.1 M NaN₃ and cytochalasin B. The amount and rate of capping could be altered by varying either the number of bound IgE molecules or the anti-IgE concentration indicating that lattice formation is required for redistribution. Monovalent Fab' fragments of the anti-IgE caused no redistribution. No endocytosis of the antibody-surface determinant complexes was observed. Under conditions adequate to inhibit cap formation on mouse lymphocytes, concanavalin A did not inhibit cap formation on the leukemic basophils.

Footnotes

¹ Present address: Department of Medicine, University of California at San Diego, San Diego, Calif. 92110.

² To whom correspondence should be addressed.