Ask about this productRelated genes to: IDO1 antibody
- Gene:
- IDO1 NIH gene
- Name:
- indoleamine 2,3-dioxygenase 1
- Previous symbol:
- IDO, INDO
- Synonyms:
- -
- Chromosome:
- 8p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-26
- Date modifiied:
- 2016-01-15
Related products to: IDO1 antibody
Related articles to: IDO1 antibody
- Dual inhibition of indoleamine 2,3-dioxygenase 1 (IDO1) and programmed death-ligand 1 (PD-L1) may alleviate suppression of antitumor immune responses by overcoming redundant immunosuppressive pathways. This study evaluated the combination of KHK2455, a novel and selective, long-lasting, and potent oral IDO1 inhibitor, with avelumab, a PD-L1 inhibitor, in adults with locally advanced or metastatic urothelial carcinoma. - Source: PubMed
Publication date: 2026/09/21
Zakharia Yousefde Spéville Bernard DogerMorales-Barrera RafaelMoreno IreneKilari DeepakPeguero JulioRao SantoshShiue Lisa HKanda HironoriLiu YiArora PayalVuppugalla RaginiRodriguez-Vida Alejo - PD-1/PD-L1 blockade can produce durable tumor control, yet primary, adaptive, and acquired resistance remain common. Existing accounts often catalogue resistance by cellular compartment, obscuring the coordinated nature of tumor adaptation. Here, we introduce immune-pressure redistribution as a treatment-oriented framework that complements cancer immunoediting by asking where therapeutic immune pressure is diverted after checkpoint release. Resistance is organized into three coupled routes: transfer into tumor-intrinsic escape through antigen-presentation loss, interferon-response defects, oncogenic rewiring, and lineage plasticity; weakening through defective priming, terminal T-cell differentiation, compensatory checkpoints, metabolic constraint, and chronic cytokine signaling; and unloading into stromal, vascular, myeloid, regulatory, microbial, and systemic host compartments. We integrate clinically validated mechanisms with emerging evidence, including the temporal duality of interferon-JAK signaling, the role of tumor-draining lymph nodes in sustaining progenitor-exhausted T cells, and the limited translation of TIGIT, IDO1, TGF-β, and CSF-1R targeting. We further propose a biomarker-guided strategy that combines tumor visibility, immune-cell state, spatial architecture, systemic inflammation, and early treatment dynamics to identify the dominant resistance topology. This framework supports topology-matched combinations and adaptive sequencing rather than uniform escalation, with the aim of restoring productive immune pressure while limiting compensatory escape and toxicity. - Source: PubMed
Publication date: 2026/09/20
Wang XiaodongLiu JiayiHairulajiang AlifujiangWang JunjieWang QianqianLi ZhiHongZou BingwenFeng Yeqian - Huntington's disease (HD) is an inherited, progressive neurodegenerative disorder caused by the expansion of the CAG repeat in the HTT (huntingtin) gene. Repeated CAG sequences in the HTT gene lead to the accumulation of a toxic form of the protein within cells that contain it. The kynurenine pathway (KP), which metabolizes the amino acid L-tryptophan, has been implicated in the pathology of HD. The enzyme indoleamine 2,3-dioxygenase 1 (IDO1) is a primary component of the KP, producing several neuroactive metabolites, including the neurotoxic metabolite quinolinic acid (QA) and 3-hydroxykynurenine (3-HK). The activity of IDO1 is associated with inflammation, oxidative damage and excitotoxicity. Structures of IDO1 (as represented in the Protein Data Bank under PDB: 2D0T) have enabled the development of inhibitors, with Exiguamine A demonstrating potent IDO1 activity. Though there are challenges with IDO1 selectivity and its penetration into the brain, IDO1 remains a promising candidate and should be further evaluated as a therapeutic target in HD. - Source: PubMed
Publication date: 2026/09/18
Malakar VishnuMalakar Chandi CMali Pratap ChandPoddar Nitesh Kumar - Interferon regulatory factor 5 (IRF5) is genetically linked to ulcerative colitis (UC) susceptibility, yet its role in intestinal inflammation remains poorly understood. Here, we detected IRF5 expression in intestinal tissues from 29 UC patients and 10 healthy controls via immunohistochemistry and immunofluorescence. We constructed DSS-induced acute colitis models in IRF5-knockout (IRF5-/-) and wild-type (IRF5+/+) mice and analyzed the transcriptome of IRF5-knockdown macrophages. IRF5 was highly upregulated in inflamed intestinal tissues of UC patients and DSS-treated mice, primarily in CD68 macrophages. Compared with wild-type mice, IRF5-/- mice exhibited attenuated colitis, with reduced weight loss, lower disease activity index scores and milder colon shortening. Moreover, IRF5 deletion increased anti-inflammatory cytokines (IL-1rn, IL-10, IL-13, IL-17) and decreased pro-inflammatory cytokines (IL-1β, TNF). Transcriptome analysis revealed that IRF5 knockdown suppressed M1 pro-inflammatory genes (Ido1, Il12b) and upregulated the M2 marker MRC2. It also markedly inhibited TLR signaling and actin cytoskeleton regulation. Additionally, IRF5 downregulation reduced Tlr2 expression, indicating a positive feedback loop between IRF5 and TLR signaling. In summary, IRF5 exacerbates intestinal inflammation by promoting M1 macrophage polarization and activating TLR signaling, making it a promising therapeutic target for UC. - Source: PubMed
Publication date: 2026/09/17
Shao LimingChen YiWu LunpoZhong Jing - Metal ions are increasingly recognized as regulators of immune function, yet their application in cancer immunotherapy remains underexplored. Here, we identified cobalt ions (Co) as potent suppressors of IFN-γ-induced IDO1 expression through systematic screening of biologically relevant metal ions. Across multiple cancer cell lines, Co notably reduced IDO1 expression and kynurenine production. Mechanistically, Co destabilized IFNGR1 and inhibited IFN-γ-JAK-STAT1 signaling, thereby restoring kynurenine/tryptophan metabolic balance and alleviating immunosuppression of CD8 T cell. These effects reprogrammed the immunosuppressive tumor microenvironment toward enhanced cytotoxic T cell activity. To minimize the toxicity associated with free Co, we developed ConaHA, a hyaluronic acid-based nanoparticle platform enabling sustained and tumor-targeted cobalt delivery. ConaHA enhanced cobalt-mediated immune checkpoint blockade in vivo, resulting in notably improved antitumor efficacy in subcutaneous Panc02, MC38, and B16F10 tumor models and KPC (; ; ) models. Collectively, these findings reveal a previously unrecognized immunoregulatory role of Co and establish a promising framework for metalloimmunotherapy through modulation of metal-immune signaling pathways. - Source: PubMed
Publication date: 2026/09/18
Jiang TianyiHuang XiaowanWu ZhixinAbudusaimaiti GulinaizaierSong YangDuan HongtaoZhou YupingChen YaoxuDu SitongZhang HaoQian JieyingZhang Yunjiao