International Immunology, Vol. 13, No. 7, 843-851,
July 2001
© 2001 Japanese Society for Immunology
Regulation of mouse mast cell surface Fc
RI expression by dexamethasone
1 Departments of Allergy and Rheumatology,
2 Bioregulatory Function, and
3 Respiratory Medicine, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
4 Allergy and Atopy Research Center, Juntendo University School of Medicine, Tokyo 113-8421, Japan
5 Division of Biochemistry and Immunochemistry, National Institute of Health Sciences, Tokyo 158-8501, Japan
6 Department of Medicine, Teikyo University School of Medicine, Tokyo 173-8606, Japan
7 Department of Pathology, Stanford University Medical Center, Stanford, CA 94305-5324, USA
Correspondence to: M. Yamaguchi
It is now clear that the mast cell's functional response to IgE-dependent stimulation can be influenced significantly by the level of expression of the high-affinity IgE receptor (Fc
RI) on the cell's surface. Thus, modulation of FcRI surface expression represents a potentially important mechanism for regulating mast cell activity in allergic reactions. In this study, we examined whether a glucocorticoid, dexamethasone (DEX), can influence levels of mast cell FcRI expression either in the presence or absence of IgE, an up-regulator of the mast cell surface FcRI level. In the absence of IgE, DEX decreased the surface FcRI levels in mouse peritoneal mast cells, mouse bone marrow-derived cultured mast cells and a mouse mast cell line, Cl.MC/C57.1. Moreover, DEX also partially suppressed the ability of IgE to enhance surface expression of FcRI in these cells. Three different glucocorticoids, DEX, methylprednisolone and hydrocortisone, suppressed FcRI expression in mast cells, whereas sex steroids, i.e. estradiol, progesterone and testosterone, did not, indicating that the FcRI-suppressing effect is glucocorticoid specific. On the other hand, DEX did not affect levels of FcRI 
, ß or 
mRNA, suggesting that its ability to decrease surface FcRI reflects a post-transcriptional mechanism. Finally, DEX-treated mast cells showed a reduced degranulation response to antigenic stimulation through down-regulation of surface FcRI expression in addition to DEX-induced changes in downstream signals. These results show that mast cell surface FcRI expression is suppressed by glucocorticoids in both the presence and absence of IgE, and suggest that reduction of mast cell surface FcRI levels may be one of the favorable anti-allergic actions of glucocorticoids.
Keywords: allergy, flow cytometry, glucocorticoids, histamine release, IgE, IgE receptor
Transmitting editor: D. Kitamura
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