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RI Induces the Tryptophan Degradation Pathway Involved in Regulating T Cell Responses1
Departments of
* Dermatology and
Psychiatry, University of Bonn, Bonn, Germany; and
Institut National de la Santé et de la Recherche Médicale Unité Etablissement Français du Sang-Alsace, Strasbourg, France
Fc
RI is suspected to play a pivotal role in the pathophysiology
of atopic disorders such as atopic dermatitis. In search for genes
differentially regulated by FcRI on APCs, a differential cDNA bank
of receptor-stimulated and unstimulated monocytes was established. By
means of suppression subtractive hybridization, we identified
kynurenine 3-monooxygenase and subsequently indoleamine 2,3-dioxygenase
(IDO) to be overexpressed in FcRI-activated monocytes. IDO is the
rate-limiting enzyme in the catabolism of the essential amino acid
tryptophan. We show that cross-linking of FcRI on monocytes results
in low tryptophan concentrations associated with impaired T cell
stimulatory capacity. Importantly, T cell suppression could be
prevented by the addition of tryptophan or inhibition of IDO. Moreover,
stimulation of T cells by FcRI-activated monocytes was increased
compared with T cell stimulation by nonactivated monocytes if exogenous
supply of tryptophan was available. We speculate that the expression of
IDO by FcRI+ APCs in vivo allows these cells to regulate
T cell responses in atopic disorders by inhibiting or stimulating T
cell proliferation, depending on the metabolic
environment.
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