Regulation of mouse mast cell surface FcεRI 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.
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- Authors
- Yamaguchi, M., Hirai, K., Komiya, A., Miyamasu, M., Furumoto, Y., Teshima, R., Ohta, K., Morita, Y., Galli, S. J., Ra, C., & Yamamoto, K.
- Affiliations
- The University of Tokyo (JP)
- Juntendo University (JP)
- National Institute of Health Sciences (JP)
- Teikyo University (JP)
- Stanford Medicine (US)
- Corresponding author
- Yamaguchi, Masao
- Venue
- International Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2001-07
- Volume
- 13
- Issue
- 7
- Pages
- 843-851
- ISSN
- 0953-8178 (ISSN-L)
- 1460-2377
- OpenAlex
- W2123350636
- Cited by
- 42
- References
- 40
- Citations by year
- 2026: 1 · 2024: 2 · 2021: 2 · 2020: 2 · 2019: 1 · 2018: 1 · 2017: 2 · 2016: 2 · 2015: 3 · 2014: 2 · 2013: 5 · 2012: 2
- FWCI
- 0.86
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- International Immunology (publishedVersion)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (R01CA072074, CA 72074)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
- Keywords
- FcεRI, mast cells, dexamethasone, glucocorticoids, IgE, receptor surface expression, mast cell degranulation, anti-allergic effects, post-transcriptional regulation, peritoneal mast cells, methylprednisolone, cortisol, sex steroids
- MeSH terms
- Animals, Cells, Cultured, Dexamethasone, Estradiol, Gene Expression Regulation, Glucocorticoids, Hydrocortisone, Immunoglobulin E, Mast Cells, Methylprednisolone, Mice, Inbred BALB C, Progesterone, RNA, Messenger, Testosterone, Receptors, IgE, Mice
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