Reverse signaling through GITR ligand enables dexamethasone to activate IDO in allergy.
作者： Ursula Grohmann , Claudia Volpi , Francesca Fallarino , Silvia Bozza , Roberta Bianchi
DOI: 10.1038/NM1563
关键词: Indoleamine 2,3-dioxygenase 、 Cancer research 、 Co-stimulation 、 Dexamethasone 、 In vivo 、 Glucocorticoid 、 Immunology 、 Ligand (biochemistry) 、 Allergy 、 Glucocorticoid-Induced TNFR-Related Protein 、 Biology
摘要: Glucocorticoid-induced tumor necrosis factor receptor (GITR) on T cells and its natural ligand, GITRL, accessory contribute to the control of immune homeostasis. Here we show that reverse signaling through GITRL after engagement by soluble GITR initiates immunoregulatory pathway tryptophan catabolism in mouse plasmacytoid dendritic cells, means noncanonical NF-κB–dependent induction indoleamine 2,3-dioxygenase (IDO). The synthetic glucocorticoid dexamethasone administered vivo activated IDO symmetric CD4+ cells. drug exerted IDO-dependent protection a model allergic airway inflammation. Modulation via GITR-GITRL coreceptor system might represent an effective therapeutic target regulation. Induction could be important mechanism underlying anti-inflammatory action corticosteroids.
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