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Decrease in IgE Fc receptor expression on mouse bone marrow-derived mast cells and inhibition of PAF-acether formation and of. beta. -hexosaminidase release by dexamethasone

Journal Article · · J. Immunol.; (United States)
OSTI ID:7092190
The effect of dexamethasone (DM) on the immunologic and nonimmunologic release of paf-acether and of the granule marker ..beta..-hexosaminidase (BHEX) from mouse bone marrow-derived mast cells (BMMC) was studied. Preincubation of BMMC with DM inhibited in a dose-dependent fashion the immunologic release of paf-acether and of BHEX as compared with control cells. The antigen-induced increase in acetyltransferase activity, used as an index of cellular activation, was inhibited by 37 +/- 16% in 1 ..mu..M DM-treated BMMC as compared with untreated cells. Preincubation of BMMC with DM for 24 hr caused a dose-dependent inhibition of /sup 125/I-IgE binding to the cells, with a half-maximal effect at 14 nM. The number of IgE Fc receptors was decreased by 55% in 1 ..mu..M DM-treated BMMC as compared with untreated cells. Cytofluorometer analysis of BMMC sensitized with a saturating amount of purified monoclonal IgE, followed by addition of a fluoresceinated anti-mouse IgG (heavy and light chains), revealed a single cellular population for both DM-treated and untreated BMMC. The possible link between the decreased sensitization of the cells consequent to the reduction in IgG Fc receptor expression and the alteration of the secretory response and acetyltransferase activity was investigated. BMMC were incubated with IgE under experimental conditions giving half-sensitization of the cells. Upon antigen challenge, a 10.5 +/- 3.7% decrease in acetyltransferase activity and a 29.2 +/- 3.5% decrease in paf-acether release were observed with half-sensitized cells as compared with cells sensitized with a saturating amount of IgE. These results indicate that DM inhibits the immunologic release of paf-acether and of BHEX from passively sensitized BMMC and decreases the IgE Fc receptor number available for sensitization. Thus, the modulation of IgE Fc receptor number could explain part of the anti-allergic properties of glucocorticosteroids.
Research Organization:
INSERM, Clamart, France
OSTI ID:
7092190
Journal Information:
J. Immunol.; (United States), Journal Name: J. Immunol.; (United States) Vol. 136:4; ISSN JOIMA
Country of Publication:
United States
Language:
English

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