title: Regulation of mouse mast cell surface Fc epsilon RI expression by dexamethasone.
abstract: 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 epsilon RI) on the cell's surface. Thus, modulation of Fc epsilon RI 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 Fc epsilon RI expression either in the presence or absence of IgE, an up-regulator of the mast cell surface Fc epsilon RI level. In the absence of IgE, DEX decreased the surface Fc epsilon RI 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 Fc epsilon RI in these cells. Three different glucocorticoids, DEX, methylprednisolone and hydrocortisone, suppressed Fc epsilon RI expression in mast cells, whereas sex steroids, i.e. estradiol, progesterone and testosterone, did not, indicating that the Fc epsilon RI-suppressing effect is glucocorticoid specific. On the other hand, DEX did not affect levels of Fc epsilon RI alpha, beta or gamma mRNA, suggesting that its ability to decrease surface Fc epsilon RI reflects a post-transcriptional mechanism. Finally, DEX-treated mast cells showed a reduced degranulation response to antigenic stimulation through down-regulation of surface Fc epsilon RI expression in addition to DEX-induced changes in downstream signals. These results show that mast cell surface Fc epsilon RI expression is suppressed by glucocorticoids in both the presence and absence of IgE, and suggest that reduction of mast cell surface Fc epsilon RI levels may be one of the favorable anti-allergic actions of glucocorticoids.
authors: Department of Allergy and Rheumatology, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
authors: M
authors: M
authors: Yamaguchi
authors: K
authors: K
authors: Hirai
authors: A
authors: A
authors: Komiya
authors: M
authors: M
authors: Miyamasu
authors: Y
authors: Y
authors: Furumoto
authors: R
authors: R
authors: Teshima
authors: K
authors: K
authors: Ohta
authors: Y
authors: Y
authors: Morita
authors: S J
authors: SJ
authors: Galli
authors: C
authors: C
authors: Ra
authors: K
authors: K
authors: Yamamoto
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D003907:Dexamethasone / Q000378:metabolism / Q000494:pharmacology*; D004958:Estradiol / Q000378:metabolism / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects*; D005938:Glucocorticoids / Q000378:metabolism / Q000494:pharmacology*; D006854:Hydrocortisone / Q000378:metabolism / Q000494:pharmacology; D007073:Immunoglobulin E / Q000276:immunology / Q000494:pharmacology; D008407:Mast Cells / Q000166:cytology / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D008775:Methylprednisolone / Q000378:metabolism / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D011374:Progesterone / Q000378:metabolism / Q000494:pharmacology; D012333:RNA, Messenger; D017455:Receptors, IgE / Q000235:genetics*; D013739:Testosterone / Q000378:metabolism / Q000494:pharmacology
chemical_list: D005938:Glucocorticoids; D012333:RNA, Messenger; D017455:Receptors, IgE; D007073:Immunoglobulin E; D013739:Testosterone; D011374:Progesterone; D004958:Estradiol; D003907:Dexamethasone; D006854:Hydrocortisone; D008775:Methylprednisolone