Modulation of high-affinity IgE receptor expression in blood monocytes: Opposite effect of IL-4 and glucocorticoids

Citation
P. Gosset et al., Modulation of high-affinity IgE receptor expression in blood monocytes: Opposite effect of IL-4 and glucocorticoids, J ALLERG CL, 107(1), 2001, pp. 114-122
Citations number
37
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
ISSN journal
00916749 → ACNP
Volume
107
Issue
1
Year of publication
2001
Pages
114 - 122
Database
ISI
SICI code
0091-6749(200101)107:1<114:MOHIRE>2.0.ZU;2-I
Abstract
Background: The expression of high-affinity IgE receptor (Fc epsilon RI) is increased in blood monocytes (BMs) from allergic patients compared with th ose of nonatopic subjects (NASs). Objective: We investigated the in vitro effect of cytokines involved in all ergic diseases on the modulation of Fc epsilon RI expression in BMs from al lergic asthmatic patients (AAPs) and NASs. The influence of in vitro and in vivo treatments with glucocorticoids (GCs) was also assessed. Methods: Fc epsilon RI alpha -chain expression on BMs evaluated by flow cyt ometry analysis was studied ex vivo in AAPs treated or not with GCs and in NASs. IgE receptor expression was also evaluated in vitro with or without s timulation by IL-4, IL-13, GM-CSF, and/or GCs, Messenger (m)RNA expression was also analyzed with RT-PCR. Results: The expression of the Fc epsilon RI alpha chain was significantly increased in BMs from untreated patients, with AAPs compared with NASs (P < .05). In steroid-treated AAPs Fc<epsilon>RI alpha -chain expression return ed to the level found in BMs from NASs. In vitro addition of IL-1 induced a dose-dependent increase in Fc epsilon RI alpha -chain expression on BMs fr om NASs, and this effect was significantly enhanced with BMs from AAPs. Fc epsilon RI alpha -chain mRNA was significantly upregulated by IL-1, whereas the beta chain was always undetectable. The gamma chain was not modulated by IL-4. Similar findings were obtained with IL-13. In contrast with CDU ex pression, GM-CSF alone or in coincubation with IL-4 had no effect on Fc eps ilon RI alpha -chain expression in BMs. Lastly, GCs significantly inhibited in vitro the IL-4-induced Fc epsilon RI alpha -chain expression (P < .05). Conclusion: Two different pathways by which Fc<epsilon>RI alpha -chain expr ession was modulated in BMs were identified: (1) the enhancing effect of IL -4 and IL-13 and (2) the inhibitory effect of GCs. Modulation of Fc epsilon RI alpha -chain expression on BMs may affect their capacity to regulate al lergic inflammation.