ArticleJournal of cellular and molecular medicine2014
Forced IDO1 expression in dendritic cells restores immunoregulatory signalling in autoimmune diabetes.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 57 citations in OpenAlex.
- Metabolomic profile differs between LADA and type 1 diabetes identifying tryptophan metabolism as a pathway involved in the heterogeneity of autoimmune diabetes.Diabetologia · 2026Article
- The Kynurenine Pathway: Unraveling Its Role in Neurological Disorders via Mammalian Cellular Models.International journal of molecular sciences · 2026Review
- Cell Signaling by Tryptophan Catabolism.Biochemistry · 2026Review
- Interferon-gamma signaling pathway: Modulation of key genes in the progression of glioblastoma.World journal of biological chemistry · 2025Review
- Microglia-specific Ido2 deficiency attenuates ictogenesis in the TMEV model of viral encephalitis.Brain, behavior, and immunity · 2025Article
- Neuroactive Kynurenines as Pharmacological Targets: New Experimental Tools and Exciting Therapeutic Opportunities.Pharmacological reviews · 2024Review
- Identification of a Compound Inhibiting Both the Enzymatic and Nonenzymatic Functions of Indoleamine 2,3-Dioxygenase 1.ACS pharmacology & translational science · 2024Article
- The role of tryptophan metabolism and tolerogenic dendritic cells in maintaining immune tolerance: Insights into celiac disease pathogenesis.Immunity, inflammation and disease · 2024Review
- Sensing of an HIV-1-Derived Single-Stranded RNA-Oligonucleotide Induces Arginase 1-Mediated Tolerance.Cells · 2024Article
- Immune regulation through tryptophan metabolism.Experimental & molecular medicine · 2023Review
- Review
- A tryptophan metabolite prevents depletion of circulating endothelial progenitor cells in systemic low-grade inflammation.Frontiers in immunology · 2023Article
- Indoleamine 2,3-dioxygenase 1 (IDO1): an up-to-date overview of an eclectic immunoregulatory enzyme.The FEBS journal · 2022Review
- Article
- The Immunomodulatory Enzyme IDO2 Mediates Autoimmune Arthritis through a Nonenzymatic Mechanism.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Leverage biomaterials to modulate immunity for type 1 diabetes.Frontiers in immunology · 2022Review
- Impact of IDO1 and IDO2 on the B Cell Immune Response.Frontiers in immunology · 2022Review
- The Kynurenine Pathway-New Linkage between Innate and Adaptive Immunity in Autoimmune Endocrinopathies.International journal of molecular sciences · 2021Review
- Class IA PI3Ks regulate subcellular and functional dynamics of IDO1.EMBO reports · 2020Article
- Role of DNA-LL37 complexes in the activation of plasmacytoid dendritic cells and monocytes in subjects with type 1 diabetes.Scientific reports · 2020Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Indoleamine 2,3-dioxygenase (IDO1), a tryptophan catabolizing enzyme, is recognized as an authentic regulator of immunity in several physiopathologic conditions. We have recently demonstrated that IDO1 does not merely degrade tryptophan and produce immunoregulatory kynurenines, but it also acts as a signal-transducing molecule, independently of its enzymic function. IDO1 signalling activity is triggered in plasmacytoid dendritic cells (pDCs) by transforming growth factor-β (TGF-β), an event that requires the non-canonical NF-κB pathway and induces long-lasting IDO1 expression and autocrine TGF-β production in a positive feedback loop, thus sustaining a stably regulatory phenotype in pDCs. IDO1 expression and catalytic function are defective in pDCs from non-obese diabetic (NOD) mice, a prototypic model of autoimmune diabetes. In the present study, we found that TGF-β failed to activate IDO1 signalling function as well as up-regulate IDO1 expression in NOD pDCs. Moreover, TGF-β-treated pDCs failed to exert immunosuppressive properties in vivo. Nevertheless, transfection of NOD pDCs with Ido1 prior to TGF-β treatment resulted in activation of the Ido1 promoter and induction of non-canonical NF-κB and TGF-β, as well as decreased production of the pro-inflammatory cytokines, interleukin 6 (IL-6) and tumour necrosis factor-α (TNF-α). Overexpression of IDO1 in TGF-β-treated NOD pDCs also resulted in pDC ability to suppress the in vivo presentation of a pancreatic β-cell auto-antigen. Thus, our data suggest that a correction of IDO1 expression may restore its dual function and thus represent a proper therapeutic manoeuvre in this autoimmune setting.
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