| Autor: |
VON BUBNOFF, D., BEZOLD, G., MATZ, H., HANAU, D., SALLE, H. De La, BIEBER, T. |
| Předmět: |
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| Zdroj: |
Clinical & Experimental Immunology; May2003, Vol. 132 Issue 2, p247-253, 7p |
| Abstrakt: |
SUMMARY 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, Fcℇ RI, is the principal receptor for the binding of specific IgE in type I-mediated allergies. We demonstrated recently that IDO is overexpressed in Fcℇ RI-stimulated monocytes. In the present study, we performed quantification of IDO gene induction after treatment of atopic (Fcℇ RIhigh ) and non-atopic (Fcℇ RIlow/– ) 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 Fcℇ RI. 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 Fcℇ RI and discloses differences thereof in atopic and non-atopic cells upon inflammatory stimuli. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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