Modulation of high-affinity IgE receptor expression in blood monocytes: opposite effect of IL-4 and glucocorticoids.
BACKGROUND
The expression of high-affinity IgE receptor (Fc epsilon RI) 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 Fc epsilon RI 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
Fc epsilon RI alpha-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 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 returned to the level found in BMs from NASs. In vitro addition of IL-4 induced a dose-dependent increase in Fc epsilon RI alpha-chain expression on BMs from NASs, and this effect was significantly enhanced with BMs from AAPs. Fc epsilon RI alpha-chain mRNA was significantly upregulated by IL-4, 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 CD23 expression, GM-CSF alone or in coincubation with IL-4 had no effect on Fc epsilon RI alpha-chain expression in BMs. Lastly, GCs significantly inhibited in vitro the IL-4-induced Fc epsilon RI alpha-chain expression (P <.05).


CONCLUSIONS
Two different pathways by which Fc epsilon RI alpha-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 Fc epsilon RI alpha-chain expression on BMs may affect their capacity to regulate allergic inflammation.
Gosset
P
P
INSERM U416, Institut Pasteur, Lille, France.
Lamblin-Degros
C
C
Tillie-Leblond
I
I
Charbonnier
A S
AS
Joseph
M
M
Wallaert
B
B
Kochan
J P
JP
Tonnel
A B
AB
D001249:Asthma / Q000097:blood / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D005938:Glucocorticoids / Q000235:genetics / Q000494:pharmacology; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000097:blood; D018793:Interleukin-13 / Q000494:pharmacology; D015847:Interleukin-4 / Q000235:genetics / Q000494:pharmacology; D009000:Monocytes / Q000737:chemistry* / Q000378:metabolism; D011505:Protein-Tyrosine Kinases / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D017455:Receptors, IgE / Q000235:genetics; D017452:Receptors, IgG / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics
D005938:Glucocorticoids; D018793:Interleukin-13; D012333:RNA, Messenger; D017455:Receptors, IgE; D017452:Receptors, IgG; D015847:Interleukin-4; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D011505:Protein-Tyrosine Kinases