Quantification of indoleamine 2,3-dioxygenase gene induction in atopic and non-atopic monocytes after ligation of the high-affinity receptor for IgE, FcɛRI and interferon-γstimulation

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Abstract
Antigen‐presenting cells (APCs) are crucial in regulating the outcome of T cell responses. Certain APCs are able to down‐regulate T cell proliferation in vitro by inducing the enzyme indoleamine 2,3‐dioxygenase (IDO) upon interferon‐γ (IFN‐γ) stimulation. IDO is the rate‐limiting enzyme in the catabolism of the essential amino acid tryptophan. A lack of extracellular tryptophan creates environments in which cells become starved for this amino acid. The high‐affinity receptor for IgE, FcɛRI, is the principal receptor for the binding of specific IgE in type I‐mediated allergies. We demonstrated recently that IDO is overexpressed in FcɛRI‐stimulated monocytes. In the present study, we performed quantification of IDO gene induction after treatment of atopic (FcɛRIhigh) and non‐atopic (FcɛRIlow/–) monocytes with IgE/anti‐IgE and IFN‐γ. By quantitative PCR ELISA, we found IDO molecule induction in atopic monocytes was enhanced about 50‐fold over non‐atopic monocytes after ligation of FcɛRI. Stimulation with IFN‐γ at a concentration of 100 U/ml in culture medium caused an increase in IDO gene copy numbers in atopics of about fourfold over that of non‐atopics. This comparative quantification study demonstrates clearly the regulation of IDO gene expression by FcɛRI and discloses differences thereof in atopic and non‐atopic cells upon inflammatory stimuli.