Human IFN-gamma R1 / IFNGR1 Protein
- Known as:
- Human Interferon-g R1 / IFNGR1 Protein
- Catalog number:
- IF1-H5223
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human IFN-gamma R1 / IFNGR1 Protein
Related genes to: Human IFN-gamma R1 / IFNGR1 Protein
- Gene:
- IFNGR1 NIH gene
- Name:
- interferon gamma receptor 1
- Previous symbol:
- IFNGR
- Synonyms:
- CD119
- Chromosome:
- 6q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: Human IFN-gamma R1 / IFNGR1 Protein
Related articles to: Human IFN-gamma R1 / IFNGR1 Protein
- 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 - Lymph node (LN) metastasis is a major determinant of prognosis in gastric cancer, yet the immune microenvironment of metastatic versus non-metastatic nodes remains incompletely defined. Spatial resolution of tumor-immune interactions may clarify mechanisms of immune escape associated with nodal progression. We performed compartment-resolved spatial transcriptomic profiling to characterize immune gene expression in gastric cancer LNs. Forty-seven formalin-fixed paraffin-embedded LNs from 13 patients with T2-T4, M0 gastric adenocarcinoma (N1-2: n = 7; N3: n = 6) were analyzed using the NanoString GeoMx Digital Spatial Profiler and an 84-gene immune pathways panel. Twenty-nine non-metastatic and 18 metastatic LNs were profiled. Regions of interest were segmented into tumor and immune compartments, yielding 65 spatially defined compartments. Differential expression was assessed across three comparisons: metastatic versus non-metastatic LNs; metastatic LNs from N1-2 versus N3 patients; and non-metastatic LNs from N1-2 versus N3 patients. Within the immune compartments, non-metastatic LNs showed higher expression of T-cell activation and checkpoint genes (CD3E, CD27, PDCD1, CTLA4), consistent with preserved immune surveillance. Metastatic LNs were enriched for WNT signaling and adhesion-related genes (CTNNB1, ITGAV) and epithelial markers (EPCAM), indicating tumor-driven immune remodeling. N3 metastatic LNs demonstrated increased ICOSLG, IL6, and IFNGR1 expression, suggesting chronic inflammatory activation and immune dysfunction. Notably, non-metastatic LNs from N3 patients upregulated antigen-presentation genes (CD74, HLA-DRB), consistent with early immune conditioning. No significant differences emerged in tumor compartments or pseudo-bulk analyses. Spatial transcriptomic profiling reveals nodal burden-associated immune remodeling, and identifies candidate biomarkers and therapeutic targets for precision immunotherapy in gastric cancer. - Source: PubMed
Publication date: 2026/09/17
Suwatthanarak ThanawatNampoolsuksan ChawisaTanjak PariyadaThanormjit KullanistAcharayothin OnchiraChaiboonchoe AmphunSuwatthanarak TharathornPithukpakorn ManopChalermwai Wipapat VickiSwangsri JirawatMethasate AsadaChinswangwatanakul VitoonParakonthun Thammawat - Secondary lymphoid organs, including the spleen, integrate innate and adaptive immune responses. Studies in murine models and humans highlight Natural Killer (NK) cells and other innate lymphoid cells (ILC) as key organizers of splenic immune activity, yet their in situ organization and interactions within immune networks are incompletely understood. Here, we report a spatially resolved single-cell atlas of human splenic NK cells and ILCs. We identify CD39TIGITCD56 NK cells that localize with alternatively activated macrophages outside of B cell follicles. Splenic ILC2s, enriched in vascular-associated regions, express CD40L and can promote B cell survival and IgA secretion. Finally, we define three spatially and functionally distinct ILC3 subsets, namely KLF2⁺ progenitor-like ILC3s, follicle-associated CD38⁺ ILC3s, and IFNGR1⁺ ILC3s, that can promote B cell proliferation, IL-10 production, and IgG class switching. This spatially resolved atlas provides a comprehensive reference of human splenic ILC organization, specialization, and interaction networks. - Source: PubMed
Publication date: 2026/08/11
Colpitts Sarah JJegatheeswaran SinthujaMashhouri SiavashHagerman AshEl-Maklizi MahmoudMurshed HumairaMak Martin LReid Kyle TMurphy Julia MMathews Jessica ARobbins Clinton SCrome Sarah Q - Mutations in genes controlling IFN-γ production or signaling underlie Mendelian susceptibility to mycobacterial disease (MSMD) and predispose affected individuals to mycobacterial and other infections. Autosomal dominant (AD) mutations in exon VI of IFNGR1, which encodes interferon-γ receptor 1 (IFN-γR1), have been associated with multifocal osteomyelitis. We report a Mexican male patient whose clinical course began with severe BCGitis at 2 years of age, followed by tuberculous lymphadenitis at age 3, disseminated tuberculosis with hepatitis at age 10, and disseminated Mycobacterium bovis infection with vertebral osteomyelitis at age 19. Subsequent manifestations included HPV-associated warts at age 21, pneumonia and vertebral osteomyelitis associated with M. colombiense at age 25, mesenteric fibrosis, hepatic abscesses, vertebral osteomyelitis associated with M. avium at age 28, and pneumonia associated with M. fortuitum at age 30. The patient responded to prolonged antimycobacterial therapy. Functional studies demonstrated deficient IL-12p40 production following BCG plus IFN-γ stimulation, impaired Stat-1 phosphorylation in response to IFN-γ, and increased cell-surface expression of CD119/IFN-γR1. Sanger sequencing identified the heterozygous IFNGR1 c.805delT (p.Tyr269Ilefs*8) variant in the patient but not in his parents, consistent with a de novo event. This truncating variant leads to cell-surface accumulation of a defective IFN-γR1 and exerts a dominant-negative effect on IFN-γ signaling. This case, together with our literature review, supports an association between impaired IFN-γ signaling due to AD IFNGR1 variants and susceptibility to recurrent infectious osteomyelitis. - Source: PubMed
Publication date: 2026/09/06
Rivero-García PamelaMartínez-Robles LuisGonzález YolandaVentura-Ayala LauraOchoa-Hein EricGamboa-Domínguez ArmandoCasanova Jean-LaurentBoisson-Dupuis StephaniePedraza-Sánchez Sigifredo - We recently reported an immune profile that stratifies patients with axial spondyloarthritis based on clinical response to secukinumab. We now undertake an exploratory study on the secukinumab nonresponder patients to determine if immunologic changes occur during their initial secukinumab treatment that could determine their next biologic response. - Source: PubMed
Pacheco AddisonRemalante-Rayco PatriciaHaroon NigilPoddubnyy DenisInman Robert D