IL4I1 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- IL4I1 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100203
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- IL4I1 antibody Polyclonal Antibodies Primary antibodies
Related genes to: IL4I1 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- IL4I1 NIH gene
- Name:
- interleukin 4 induced 1
- Previous symbol:
- -
- Synonyms:
- FIG1
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-20
- Date modifiied:
- 2016-01-15
Related products to: IL4I1 antibody Polyclonal Antibodies Primary antibodies
Related articles to: IL4I1 antibody Polyclonal Antibodies Primary antibodies
- Metabolic hijacking of tryptophan (Trp) via the IL4I1-AHR axis is a pivotal immune evasion mechanism in cancers, yet therapeutic strategies to disrupt this pathway remain unexplored. Here, we report the identification of ZY-MY-111, a selective small-molecule inhibitor of interleukin-4-induced-1 (IL4I1), through an in-house compound library screening and structural optimization. ZY-MY-111 exhibits potency (IC = 1.86 ± 0.13 μM) in blocking IL4I1-mediated oxidative deamination. Mechanistically, ZY-MY-111 acts as a mixed-type inhibitor, competitively occupying the catalytic pocket of IL4I1 and disrupting Trp-AHR signaling in cells. Functionally, ZY-MY-111 promotes T cell proliferation, enhancing immune responses against the tumor cells. In syngeneic tumor models, ZY-MY-111 achieved 49% tumor growth inhibition in CT26 colon carcinoma (P < 0.001) and 56% tumor growth inhibition in A20 lymphoma (P < 0.001) by remodeling the immunosuppressive microenvironment: increasing CD8/CD4 T cell ratios, reducing myeloid-derived suppressor cells (MDSCs, 59% decrease), and enhancing effector memory T cell infiltration. Our findings position IL4I1 inhibition as a potential strategy to restore anti-tumor immunity. - Source: PubMed
Publication date: 2026/06/08
Li Ju-FeiWang HaoKang LingXu Cheng-ChengLiu Yuan-ChunLi Zi-XuanLin Shao-HaoWang Ming-ZhiXu Xiao-MinWang Pei-PeiYin Wan-ChaoZhou Yu-BoZhou YuLi Jia - Tryptophan (Trp) metabolism sits at the intersection of nutrition, the microbiome, mucosal immunity, and tumor adaptation. The broad observation that microbial indoles can support barrier function, whereas tumors exploit kynurenine-pathway metabolism to suppress immunity, is already established in publications. The specific contribution of this review is to organize that literature into a context- and network-based translational framework. Rather than treating indoleamine 2,3-dioxygenase 1 (IDO1) as a single bottleneck, we frame tumor Trp metabolism as a compensatory system linking IDO1, tryptophan 2,3-dioxygenase (TDO2), interleukin-4-induced gene 1 (IL4I1), amino-acid transport, amino-acid stress sensing, and downstream aryl hydrocarbon receptor (AHR) signaling. In healthy tissue, especially the gut, dietary Trp and microbiota-derived indoles can promote epithelial integrity, interleukin-22 (IL-22)-associated programs, and mucosal restraint. In tumors, the same substrate pool is redirected toward Kynurenine, kynurenic acid, indole-3-pyruvate, and related catabolites that impair cytotoxic lymphocytes, expand regulatory T-cell (Treg) and suppressive myeloid compartments, and reinforce invasion and treatment resistance. We also argue that the potential metabolite biomarker interpretation should be context-dependent. Finally, we propose a clinical-context-specific framework for intervention. Dietary and microbiome-based strategies may be most effective in prevention, premalignant states, or supportive care, whereas established cancers are more likely to require biomarker-guided targeting of tumor-associated catabolic pathways and convergent signaling mechanisms. The "paradox" is therefore not that Trp changes chemistry across settings, but that the same nutrient is routed through different cellular contexts, enzymes, ligands, and cell states. - Source: PubMed
Publication date: 2026/05/12
Cho AlexisWu ChunjingTheodoropoulos GeorgeNagarajan ManojavanMurphy Adeline MHeller Karli FSavaraj NiramolLampidis Theodore JWangpaichitr Medhi - High-risk neuroblastoma (NB) is driven by the amplification of MYCN in conjunction with additional oncogenic mutations in genes encoding kinases such as ALK. NB cells require antioxidant responses to maintain redox balance and are highly sensitive to ferroptosis. Here, we show that metabolites derived from infiltrating immune cells expressing IL4i1, a secreted oxidoreductase, are potent suppressors of NB ferroptosis. IL4i1 metabolites (indole-3-pyruvate and 4-hydroxyphenylpyruvate) blocked ferroptosis in all human NB cell lines via a mechanism that depended on free radical scavenging and NRF2 activation but did not require the aryl hydrocarbon receptor. Supernatant transfer experiments confirmed that IL4i1 creates a milieu that protects NB cells from oxidative cell death. Importantly, mice lacking IL4i1 were protected from NB in a high-penetrance MYCN and mutant ALK-driven autochthonous cancer model. Therefore, we propose that immune IL4i1 is permissive for NB growth and survival. IL4i1 produces context-dependent oncometabolites and, as a secreted enzyme, represents a target for cell death manipulation in cancers sensitive to oxidative stress-driven cell death. - Source: PubMed
Publication date: 2026/05/22
Guyot CamilleVan de Velde Lee-AnnKainacher LisaRuoff JohannaBici AnaPeterson Nicolas BernardOgger Patricia PAllen E KaitlynnSteigenberger BarbaraYeroslaviz AssaYang JunZeitler LeonieThomas Paul GMurray Peter J - Infectious diseases exacerbate atherosclerosis-associated morbidity and mortality by inducing sustained inflammatory responses characterized by elevated IL-6, TNF-α, IFN-γ, and CXCL10. Persistent CXCL10-driven recruitment of CXCR3⁺ immune cells promotes endothelial dysfunction and atherosclerotic progression. Although mesenchymal stem cells (MSCs) respond to inflammatory cues and secrete CXCL10, the contribution of CXCL10/CXCR3 signaling to intrinsic MSC immunomodulatory programming remains poorly understood. The objective of this study is to investigate whether CXCL10 signaling can modulate MSC-mediated immunoregulation. To address this, Wharton's jelly-derived MSCs (WJ-MSCs) were genetically engineered to express a membrane-anchored CXCL10-Lactadherin C1/C2 fusion protein (CXCL10-LACTC1/C2). This strategy was designed to recapitulate physiological, localized, and sustained CXCL10 signaling, enabling spatially restricted chemokine presentation that more closely mimics cell-associated CXCL10 in inflammatory microenvironments compared with soluble CXCL10. The Lactadherin C1/C2 domain was selected to achieve stable, physiological membrane anchoring without introducing artificial transmembrane domains or compromising CXCL10 bioactivity. CXCL10-LACTC1/C2-expressing MSCs exhibited increased expression of key immunoregulatory mediators, including IDO1, TGF-β1, and IL4I1. Furthermore, conditioned medium derived from these MSCs attenuated TNF-α-induced inflammatory responses in human umbilical vein endothelial cells (HUVECs), as indicated by the modulation of endothelial activation and homeostasis markers (ICAM-1, PECAM-1, KDR, vWF, and NRF2) and improvement of cell viability. Collectively, these findings provide mechanistic insight into CXCL10-mediated MSC immunoregulation and support further investigation of MSC-based and cell-free therapeutic strategies aimed at mitigating CXCL10-driven endothelial inflammation in infection-associated vascular injury and atherosclerotic disease progression. - Source: PubMed
Publication date: 2026/05/22
Molo KayaEge RukenAti̇k KübraÇıtak ElifÇulcuoğlu OrçunDarıcı HakanOrdu Emel - Oncolytic vaccinia virus JX-594 (pexastimogene devacirepvec) selectively replicates in tumour cells and stimulates antitumour immunity; however, its therapeutic potential in gastric cancer (GC) has not been systematically evaluated. In this study, we investigated the antitumour activity of JX-594 across a panel of 49 molecularly characterized GC cell lines and a xenograft mouse model and explored molecular features associated with viral sensitivity. JX-594 induced cytopathic effects (median effective dose, ED, 0.37 MOI (multiplicity of infection)) in a subset of gastric cancer cell lines and significantly suppressed tumour growth in vivo. Sensitivity to JX-594 varied across molecular subtypes, with microsatellite instability-high (MSI-H) cell lines showing greater susceptibility, whereas Epstein-Barr virus (EBV)-associated cell lines were relatively resistant. Transcriptomic analysis identified candidate biomarkers associated with viral sensitivity, including upregulated genes involved in G-protein signalling (GPR87, GRPR, PRDX5, MX1), interleukin production (IL1A, IL4I1), and vascular activation/dysfunction (OLR1, MMRN2), and downregulation of metastasis-related GAL3ST2. Notably, JX-594 activity was not correlated with TK1 or EGFR expression, suggesting additional determinants of viral susceptibility in GC. These findings provide preclinical evidence that molecular heterogeneity influences the response of GC to oncolytic virotherapy and support further investigation of JX-594 as a potential therapeutic strategy for gastric cancer. - Source: PubMed
Publication date: 2026/05/19
Kim Jee HungKim YeLinShin YoukeunPark InhoKwon Woo SunKim Tae SooLee NamheeOh KeunheeKim ChanJeung Hei-CheulRha Sun Young