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
- Indoleamine 2,3-dioxygenase 1 (IDO1) is an intracellular heme-dependent enzyme that catalyzes the initial oxidation of L-tryptophan into the kynurenine pathway, thereby linking tryptophan metabolism to immune regulation. IDO1 expression is mainly induced by interferon-γ during immune activation and inflammation, and its activity helps control immune responses through tryptophan depletion and the generation of immunomodulatory metabolites. Because of its central role in immunometabolism, IDO1 has been widely investigated as a therapeutic target, and several strategies have been developed to inhibit its enzymatic activity or reduce its functional contribution to immune suppression. However, increasing evidence indicates that IDO1 inhibition may not completely interrupt tryptophan catabolism or downstream immunoregulatory signaling. Instead, IDO1 blockade can be accompanied by compensatory mechanisms that preserve metabolic and immune regulatory outputs. These mechanisms may include activity or upregulation of alternative tryptophan-catabolizing enzymes such as TDO2, IDO2, and IL4I1; metabolic diversion toward serotonin and melatonin pathways; microbiota-derived indole production; and cell-type-specific metabolic rewiring. Therefore, understanding these adaptive responses is essential for interpreting the limited efficacy of IDO1-targeted approaches and for improving therapeutic strategies directed at tryptophan metabolism. This review discusses the main compensatory pathways that may emerge under IDO1 inhibition and their relevance to developing more effective immunometabolic interventions. - Source: PubMed
Publication date: 2026/09/12
Gontijo IsabelaCamurça MarianaKfoury José Roberto - Nasopharyngeal carcinoma (NPC) is a common malignancy with a high incidence in Southern China and Southeast Asia. Distant metastasis remains a major cause of poor prognosis. This study aims to explore the genomic and immune microenvironmental changes in primary and metastatic NPC through longitudinal analysis, to provide insights for guiding precision treatment strategies. - Source: PubMed
Publication date: 2026/08/27
Lu YingHan TiantianWang LihuiChen XishanLin HuanWang MengxiaoChen DongshengHuang Haixin - pneumonia (PCP) remains a major cause of morbidity and mortality in immunocompromised individuals. Although baicalin (Ba), a natural bioactive flavonoid, has demonstrated protective and therapeutic effects against PCP, its molecular mechanisms remain undefined. We employed dual RNA sequencing (dual RNA-seq) to characterize host and pathogen transcriptional responses to Ba treatment in an immunosuppressed rat model of PCP. - Source: PubMed
Publication date: 2026/08/26
Xue TingFan LijuanDu WeiqinChen XingxuLiu ChaofengDai WenjuanXu JiaChen LufengRen Shouan - Immune checkpoint blockade (ICB) benefits only a minority of patients with triple-negative breast cancer (TNBC), partly because tryptophan catabolism through indoleamine 2,3-dioxygenase 1 (IDO1) and tryptophan 2,3-dioxygenase 2 (TDO2) generates kynurenine, activates aryl hydrocarbon receptor (AhR) signaling, and suppresses CD8 T-cell function. We investigated whether tanshinone IIA (Tan-IIA) modulates this pathway. - Source: PubMed
Publication date: 2026/08/25
Qiu ZhuMeng ChaoTang Maocai - Systemic lupus erythematosus (SLE) is a debilitating autoimmune disease fueled by abnormal immune responses and metabolic dysregulation, often leading to life-threatening lupus nephritis (LN). While Cyclosporine A (CsA) is a potent therapeutic agent, its clinical utility is severely constrained by systemic off-target toxicity and the necessity for frequent, high-dose administration. This study evaluates P2Ns-GA-CsA, a receptor-mediated, targeted nanoparticle formulation designed to modulate the core immune-metabolic axis in LN. Using an NZBWF1/J murine model, the administration of P2Ns-GA-CsA achieves enhanced renal protection compared to conventional oral CsA (Neoral), effectively suppressing serum creatinine, clusterin, and proinflammatory cytokines while preserving renal histoarchitecture. This therapeutic efficacy is realized with less than half the dosing frequency of the clinical standard, requiring 42 doses versus 98 doses over a 14 week period. Mechanistically, P2Ns-GA-CsA treatment is associated with the restoration of gut microbial homeostasis through the enrichment of protective taxa (Lactobacillus and Muribaculaceae), facilitating a metabolic shift. This modulation of the gut-microbial metabolic axis promotes the anti-inflammatory indole pathway while suppressing the pathogenic indoleamine 2,3-dioxygenase 1 (IDO1)-kynurenine pathway. These findings demonstrate that this targeted nanotherapeutic strategy decouples the immunosuppressive benefits of CsA from its systemic toxicity while restoring gut-renal integrity in autoimmune disorders. - Source: PubMed
Babalola Kabirat TGanugula RaghuArora MeenakshiAgarwal Sandeep KMohan ChandraMehrara Babak JKumar M N V Ravi