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_4
Snippet: CTLA-4-binding also promote IDO in tumor contexts, but the enzyme has reveal activity in only a minor DC subpopulation expressing the marker CD19, but none of the pDC classical markers [32], [33]. IDO enzymatic functions in tumor dLN-sorted pDCs have been correlated to in vitro Treg differentiation and suppressive functions [24], [34]. More recently, Pallotta and colleagues described that IDO+ pDCs induced long-lived Tregs by using a TGF-β-depen.....
Document: CTLA-4-binding also promote IDO in tumor contexts, but the enzyme has reveal activity in only a minor DC subpopulation expressing the marker CD19, but none of the pDC classical markers [32], [33]. IDO enzymatic functions in tumor dLN-sorted pDCs have been correlated to in vitro Treg differentiation and suppressive functions [24], [34]. More recently, Pallotta and colleagues described that IDO+ pDCs induced long-lived Tregs by using a TGF-β-dependent pathway distinct from the catalytic activity of the enzyme. In mouse a model of skin delayed-type hypersensitivity, they shown that whereas IFN-γ-dependent IDO enzymatic activity in pDCs leads to T cell anergy, TGF-β induced IDO phosphorylation results in increased Treg frequencies [35].
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