Abstract
Background: The expression of high-affinity IgE receptor (FcϵRI) is increased in blood monocytes (BMs) from allergic patients compared with those of nonatopic subjects (NASs). Objective: We investigated the in vitro effect of cytokines involved in allergic diseases on the modulation of FcϵRI expression in BMs from allergic asthmatic patients (AAPs) and NASs. The influence of in vitro and in vivo treatments with glucocorticoids (GCs) was also assessed. Methods: FcϵRI α-chain expression on BMs evaluated by flow cytometry 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 stimulation 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 FcϵRI α chain was significantly increased in BMs from untreated patients, with AAPs compared with NASs (P < .05). In steroid-treated AAPs FcϵRI α-chain expression returned to the level found in BMs from NASs. In vitro addition of IL-4 induced a dose-dependent increase in FcϵRI α-chain expression on BMs from NASs, and this effect was significantly enhanced with BMs from AAPs. FcϵRI α-chain mRNA was significantly upregulated by IL-4, whereas the β chain was always undetectable. The γ chain was not modulated by IL-4. Similar findings were obtained with IL-13. In contrast with CD23 expression, GM-CSF alone or in coincubation with IL-4 had no effect on FcϵRI α-chain expression in BMs. Lastly, GCs significantly inhibited in vitro the IL-4–induced FcϵRI α-chain expression (P < .05). Conclusion: Two different pathways by which FcϵRI α-chain expression 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 FcϵRI α-chain expression on BMs may affect their capacity to regulate allergic inflammation. (J Allergy Clin Immunol 2001;107:114-22.)
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