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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by MacGlashan, D. Articles by Lichtenstein, L. M. Search for Related Content PubMed PubMed Citation Articles by MacGlashan, D., Jr Articles by Lichtenstein, L. M. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  In Vitro Regulation of FcRI Expression on Human Basophils by IgE Antibody Donald MacGlashan Jr, Jane McKenzie-White, Kristine Chichester, Bruce S. Bochner, Frances M. Davis, John T. Schroeder, and Lawrence M. Lichtenstein From the Johns Hopkins Asthma and Allergy Center, Baltimore, MD; and Tanox Biosystems, Inc, Houston, TX. In vivo studies suggested the possibility of an IgE-dependent regulation of high-affinity (FcRI) IgE receptor expression on basophils. The current studies extend these observations to in vitro cultures of human basophils. Incubation of basophils for 3 to 4 weeks resulted in a slow dissociation of IgE antibody, during which time FcRI expression decreased, as measured by flow cytometry using the anti-FcRI monoclonal antibody, 22E7, or by measuring FcRI mass by Western blotting of whole-cell lysates. Culture of basophils with IgE resulted in upregulation of FcRI expression by both flow cytometry and Western blotting of whole-cell lysates. Upregulation followed a linear time course during 2 weeks of culture. The relative increase in FcRI density depended on the starting density; with starting densities of FcRI of 10,000 to 170,000 per basophil, the upregulation varied 20- to 1.1-fold, respectively. Upregulation occurred in high-purity basophils, was not influenced by IgG at concentrations up to 1 mg/mL, and was inhibited by dimeric IgE. Heat-inactivated IgE was less effective and the monoclonal antibody CGP51901 that prevents IgE binding to FcRI blocked the ability of IgE to induce upregulation. The dose-response curve for IgE-induced upregulation had an effective concentration50 of 230 ng/mL. Although the receptor through which IgE induces this upregulation is not yet known, several characteristics suggest that the upregulation is mediated by IgE interacting through FcRI itself. Blood, Vol. 91 No. 5 (March 1), 1998: pp. 1633-1643 © 1998 by The American Society of Hematology. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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