Author: Lippens, Carla; Duraes, Fernanda V.; Dubrot, Juan; Brighouse, Dale; Lacroix, Mathilde; Irla, Magali; Aubry-Lachainaye, Jean-Pierre; Reith, Walter; Mandl, Judith N.; Hugues, Stéphanie
Title: IDO-orchestrated crosstalk between pDCs and Tregs inhibits autoimmunity Document date: 2016_12_23
ID: sl8148ap_3
Snippet: Indoleamine 2,3-dioxygenase (IDO) is an immunomodulatory enzyme involved in the initial and the rate-limiting step of tryptophan catabolism. Upon inflammation, IDO production has been shown to compromise T cell proliferation, promote T cell anergy and Tregs [24], [25], [26]. Depending on the experimental context, IDO can be induced either by IFN-γ, IFN-α/β, or TGF-β. CTLA-4 binding to cell-surface expressed costimulatory molecules promotes ID.....
Document: Indoleamine 2,3-dioxygenase (IDO) is an immunomodulatory enzyme involved in the initial and the rate-limiting step of tryptophan catabolism. Upon inflammation, IDO production has been shown to compromise T cell proliferation, promote T cell anergy and Tregs [24], [25], [26]. Depending on the experimental context, IDO can be induced either by IFN-γ, IFN-α/β, or TGF-β. CTLA-4 binding to cell-surface expressed costimulatory molecules promotes IDO production by pDCs through IFN-γ or IFN-α/β signalling [27], [28], [29], [30]. Furthermore CD200-Ig binding to his cognate receptor induces IDO in an IFN-α/β dependent signalling pathway [31]. Both IFN-γ and IFN-α/β pathways result in IDO+ immunosuppressive effects which are closely dependent on the catalytic activity of the enzyme.
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