Indoleamine 2,3-dioxygenase is a signaling protein in long-term tolerance by dendritic cells

التفاصيل البيبلوغرافية
العنوان: Indoleamine 2,3-dioxygenase is a signaling protein in long-term tolerance by dendritic cells
المؤلفون: Claudia Volpi, Carmine Vacca, Francesca Fallarino, Roberta Bianchi, Cinzia Brunacci, Louis Boon, Giuseppe Servillo, Maria Laura Belladonna, Ciriana Orabona, Fabio Grassi, Silvio Bicciato, Maria C. Fioretti, Paolo Puccetti, Ursula Grohmann, Mario Calvitti, Emilia Maria Cristina Mazza, Maria Teresa Pallotta
المصدر: Nature Immunology. 12:870-878
بيانات النشر: Springer Science and Business Media LLC, 2011.
سنة النشر: 2011
مصطلحات موضوعية: Immunology, Inflammation, Adaptive Immunity, Biology, T-Lymphocytes, Regulatory, IDO, Interferon-gamma, Mice, Transforming Growth Factor beta, Immunity, Hypersensitivity, Immune Tolerance, medicine, Animals, Humans, Indoleamine-Pyrrole 2,3,-Dioxygenase, Immunology and Allergy, Inducer, Indoleamine 2,3-dioxygenase, indoleamine 2, 3-dioxygenase, tryptophan catabolism, dendritic cells, immune regulation, Mice, Knockout, Mice, Inbred BALB C, Tryptophan, Immunoregulation, hemic and immune systems, Dendritic Cells, Phenotype, Cell biology, medicine.symptom, Signal transduction, Intracellular, Signal Transduction, Transforming growth factor
الوصف: Regulation of tryptophan metabolism by indoleamine 2,3-dioxygenase (IDO) in dendritic cells (DCs) is a highly versatile modulator of immunity. In inflammation, interferon-γ is the main inducer of IDO for the prevention of hyperinflammatory responses, yet IDO is also responsible for self-tolerance effects in the longer term. Here we show that treatment of mouse plasmacytoid DCs (pDCs) with transforming growth factor-β (TGF-β) conferred regulatory effects on IDO that were mechanistically separable from its enzymic activity. We found that IDO was involved in intracellular signaling events responsible for the self-amplification and maintenance of a stably regulatory phenotype in pDCs. Thus, IDO has a tonic, nonenzymic function that contributes to TGF-β-driven tolerance in noninflammatory contexts.
تدمد: 1529-2916
1529-2908
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bdd201742d404bb1bdbe4e8cbd8a42ddTest
https://doi.org/10.1038/ni.2077Test
حقوق: CLOSED
رقم الانضمام: edsair.doi.dedup.....bdd201742d404bb1bdbe4e8cbd8a42dd
قاعدة البيانات: OpenAIRE