Human CXCL10 ELISA kit
- Known as:
- Human CXCL10 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- LF-EK50717
- Product Quantity:
- 1
- Category:
- Elisa Kits
- Supplier:
- Abfron
- Gene target:
- Human CXCL10 ELISA kit
Related genes to: Human CXCL10 ELISA kit
- Gene:
- CXCL10 NIH gene
- Name:
- C-X-C motif chemokine ligand 10
- Previous symbol:
- INP10, SCYB10
- Synonyms:
- IFI10, IP-10, crg-2, mob-1, C7, gIP-10
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-09
- Date modifiied:
- 2016-10-05
Related products to: Human CXCL10 ELISA kit
Related articles to: Human CXCL10 ELISA kit
- Ulcerative colitis (UC) is a chronic relapsing inflammatory bowel disease with complex pathogenesis and limited treatments. Hemp seed oil, with its unique ω-6/ω-3 polyunsaturated fatty acid ratio and phenolic antioxidants, exhibits anti-inflammatory and gut barrier-enhancing properties, though its mechanisms in UC are not fully understood. Here, we applied an integrated transcriptomics and metabolomics approach to investigate the effects of hemp seed oil in dextran sulfate sodium (DSS)-induced UC mice. Treatment with hemp seed oil (1 g/kg) significantly alleviated disease activity, suppressed proinflammatory cytokine levels (interleukin (IL)-6, IL-1β, and IL-17), and improved colonic histopathology. Metabolomic profiling via ultrahigh-performance liquid chromatography-quadrupole-orbitrap tandem mass spectrometry (UPLC-Q-Orbitrap MS/MS) identified 19 significantly altered colonic metabolites, predominantly involved in amino acid metabolism, energy homeostasis, and lipid signalling pathways. Transcriptomic analysis suggested that hemp seed oil treatment was associated with inhibition of the IL-17 and tumor necrosis factor (TNF) signalling pathways while upregulating genes involved in barrier function (e.g., zonula occludens-1 (ZO-1) and Occludin). Integrative analysis revealed strong inverse correlations between key metabolites (e.g., docosahexaenoic acid ethyl ester, adenosine diphosphate (ADP)) and IL-17 pathway activation (IL17A, C-X-C motif chemokine ligand 10 (CXCL10)), suggesting that hemp seed oil may attenuate UC through reprogramming the "metabolism‒inflammation" axis. These findings suggest potential multitarget therapeutic mechanisms of hemp seed oil against UC, indicate critical links between metabolic reprogramming and the immune‒inflammatory axis, and offer novel insights for the development of phytomedicine for the treatment of inflammatory bowel disease. - Source: PubMed
Publication date: 2026/09/21
Zhang YujieGuan YiyunZhou JunjieYang JingLu HailongLi LixiZou ZhongjieGong Mengjuan - Immune checkpoint inhibitors (ICIs) have transformed cutaneous melanoma therapy, yet 50% of patients show primary or acquired resistance, and current biomarkers (PD-L1 and tumor mutational burden) lack precision. High-frequency ultrasound (HFUS), contrast-enhanced ultrasound (CEUS), and shear-wave elastography (SWE) are inexpensive and repeatable, but their relationship to the immune transcriptome and ICI outcomes is unknown. - Source: PubMed
Publication date: 2026/09/07
Peng JinyuDai BowenZe KanYang Jie - The Stimulator of Interferon Genes (STING) pathway plays a central role in anti-tumor immunity by mobilizing both the innate and adaptive immunity. However, hypoxia, a tumor hallmark was shown to severely constrain immune responses and lead to suboptimal therapeutic efficacy. Through bioinformatic analyses, we revealed that hypoxia directly repress STING-pathway-related genes. Furthermore, we developed tumor-targeted pH-responsive nanoparticles (SPF) to overcome hypoxia-induced STING dysfunction for amplifying immune responses. The nanoparticles (NPs) effectively accumulate and reoxygenate the hypoxic tumor, achieving a potent STING activation with enhanced secretion of type-I IFNs and other inflammatory cytokines. Moreover, SPF are capable of decreasing Tregs and polarizing M2 to M1 macrophages, thus creating an immune-promoting microenvironment to unleash cascade immune response. In colon cancer models, SPF NPs strongly inhibited tumor growth with 33% tumor-free over 50 days and long-term immune memory. Importantly, robust STING activation was achieved in human tumor samples with a substantial 782.3-fold of IFN- and 1683.8-fold CXCL10 over control, highlighting the significance of hypoxia overcoming on STING activation in clinical settings. This study demonstrates a tumor-responsive nanomedicine with precise spatiotemporal control of hypoxia relief to overcome STING resistance, guiding the rational design and clinical translation of therapeutics for next-generation cancer immunotherapy. - Source: PubMed
Publication date: 2026/06/25
Hai LinnaWang JianLiu DanYun KaiqingMa KongshuoPeng YuxuanXu MengdiMa XinboGao ShanWang QinZhou JiahuiLiang ShuangWang Zhaohui - Macrophages are key regulators of innate and adaptive immune responses through antigen presentation and the production of inflammatory mediators and growth factors. Imbalances in the activation and inhibition of pro-inflammatory type 1-like macrophages (M1) and anti-inflammatory type 2-like macrophages (M2) are closely associated with various autoimmune and chronic inflammatory diseases, underscoring the need for targeted therapeutic approaches. Numerous studies have shown that sulfated polysaccharides from marine algae, especially fucoidans from brown algae, exhibit a wide range of anti-inflammatory activities. This study aims to investigate the anti-inflammatory mode of action of algae-derived fucoidans in monocyte-derived macrophages and to identify the key regulatory proteins and inflammatory mediators involved. - Source: PubMed
Publication date: 2026/09/03
Ostermann JasminGemoll TimoSchnüttgen TabeaTischhöfer Marie-TheresPlötze-Martin KirstinFleckner JonasBruchhage Karl-LudwigAlban SusannePries Ralph - Colorectal cancer immunotherapy remains limited by insufficient innate immune activation, poor tumor immune infiltration, and resistance to immune checkpoint blockade. Herein, we developed a KAT6A inhibitor-loaded and anti-PD-L1-coated manganese metal-organic framework (MnMOF) nanoplatform for enhanced colorectal cancer immunotherapy through coordinated cGAS-STING activation and PD-L1 blockade. The KAT6A inhibitor (Ki) PF-9363 was loaded into MnMOF, followed by surface modification with anti-PD-L1 antibody to obtain Ki@MnMOF@P. The nanoplatform exhibited efficient Ki loading, pH-responsive drug release, and retained PD-L1 blocking activity. In vitro, Ki@MnMOF@P showed enhanced cellular uptake and selective cytotoxicity against HCT116 cells while maintaining low toxicity toward normal colonic epithelial NCM460 cells. In a CT26 colorectal tumor-bearing mouse model, systemic administration of Ki@MnMOF@P significantly inhibited tumor growth, reduced tumor weight, and prolonged survival. Moreover, Ki@MnMOF@P achieved favorable tumor accumulation without obvious systemic toxicity. Mechanistically, Ki@MnMOF@P suppressed KAT6A expression, promoted cGAMP production, enhanced cGAS expression, and increased STING phosphorylation in tumor tissues. Besides, the nanoplatform remodeled the tumor immune microenvironment by elevating IFN-β, CXCL10, TNF-α, IL-6, and IFN-γ levels and increasing CD8 and CD4 T-cell infiltration. These findings demonstrate that Ki@MnMOF@P integrates KAT6A inhibitor and manganese-mediated cGAS-STING activation and anti-PD-L1-mediated checkpoint blockade, providing a promising nanomedicine strategy for colorectal cancer immunotherapy. - Source: PubMed
Publication date: 2026/09/06
Wang HeleiJi ChaoXie ChengLi ZongyangCai Hongqiao