Mouse CXCL16 ELISA kit
- Known as:
- Mouse CXCL16 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- LF-EK50573
- Product Quantity:
- 1×96T
- Category:
- Peptides
- Supplier:
- Abfron
- Gene target:
- Mouse CXCL16 ELISA kit
Ask about this productRelated genes to: Mouse CXCL16 ELISA kit
- Gene:
- CXCL16 NIH gene
- Name:
- C-X-C motif chemokine ligand 16
- Previous symbol:
- -
- Synonyms:
- SR-PSOX, CXCLG16, SRPSOX
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-21
- Date modifiied:
- 2016-10-05
Related products to: Mouse CXCL16 ELISA kit
Related articles to: Mouse CXCL16 ELISA kit
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Publication date: 2026/06/09
Shang ChenWang YanruChen QiuhongWu JuecenWang Yanguo - Hepatitis B virus (HBV) may alter immunotherapy responsiveness in HBV-positive hepatocellular carcinoma (HCC) patients. However, the underlying immune mechanisms remain unclear. To characterize the immune determinants underlying the enhanced immunotherapy response observed in HBV HCC patients, we comprehensively analyzed 528 HCC patients who received immunotherapy, encompassing diverse hepatitis infections. We performed an analysis incorporating single-cell RNA sequencing, spatial transcriptomics, and tissue microarray validation to map the tumor immune landscape. An adoptive T cell transfer combined with anti-programmed death-1 (PD-1) therapy in a syngeneic HCC mouse model was performed to validate key findings. HBV HCC patients exhibited superior responses to immunotherapy and prolonged overall survival. Remarkably, HBV HCC patients harbored an elevated proportion of exhausted CD8 T cells, and these cells concurrently exhibited enhanced immune activity and cytotoxic potential. Our study spotlighted a novel subset of exhausted CD8 T cells, termed PD-1 CXCR6 CD8 T cells. In untreated cases, high levels of PD-1 CXCR6 CD8 T cells correlated with poor prognosis. In contrast, among patients receiving immunotherapy, their enrichment was associated with markedly better outcomes. , adoptive transfer of CXCR6 T cells markedly augmented the antitumor efficacy of anti-PD-1 therapy. Moreover, PD-1 CXCR6 CD8 T cells demonstrated a prominent interaction with CXCL16 macrophages in HBV HCC. Taken together, we identified a novel exhausted T cell subset, PD-1 CXCR6 CD8 T cells, that are enriched in HBV HCC patients and maintained by CXCL16 macrophages. The enrichment of PD-1 CXCR6 CD8 T cells and their interaction with CXCL16 macrophages may contribute to the enhanced immunotherapy response observed in HBV HCC. - Source: PubMed
Publication date: 2026/01/20
Yang RanzhiqiangLu CongyuJian QianSong YinghuiSun BoHe WeiLi JieqiongYang FanWang XiaohuiTan ZhiguoYang JiajinYu ChunzhaoPeng ChuangYin YulongGao YuanHe LiuqinZou LianhongLiu Sulai - Juvenile-onset recurrent respiratory papillomatosis (JORRP) is a rare, human papillomavirus (HPV)-driven pediatric disease characterized by recurring papillomas in the respiratory tract. The contribution of dysregulated T-cell immunity to disease severity remains poorly understood. This study included 97 JORRP patients and 124 controls. Due to sample limitations, downstream analyses, including flow cytometry, TCR, and RNA sequencing, were performed on distinct patient subsets (detailed in Methods). We identified a selective expansion of TCR Vβ3 T cells, including expanded TRBV28 clonotypes, in patients with aggressive disease. These T cells exhibited heightened cytotoxicity and activation markers, and were enriched in papilloma tissues. Within the tumor microenvironment, gene expression profiling revealed upregulated chemokine signaling pathways (CCR2/CCL7, CXCR6/CXCL16) and key immunosuppressive markers, including PD-L1 and TGF-β1. Our findings demonstrate a tumor-specific clonal expansion and functional alteration of TCR Vβ3 T cells in JORRP, suggesting these pathways as preliminary targets for further investigation.IMPORTANCEOur study identifies a disease-specific T-cell signature in juvenile-onset recurrent respiratory papillomatosis (JORRP), marked by the clonal expansion of TCR Vβ3 T cells with distinct TRBV28-dominant clonotypes. These T cells exhibit heightened cytotoxic potential and activation markers but appear functionally constrained within an immunosuppressive tumor microenvironment. Additionally, we discovered a dysregulated chemokine axis (CCR2/CCL7 and CXCR6/CXCL16), which likely facilitates T-cell recruitment, yet fails to sustain their antiviral activity. These findings provide mechanistic insights into why HPV-driven papillomas persist despite immune infiltration. Importantly, our work suggests that targeting TCR Vβ3 T-cell responses and modulating key chemokine pathways could offer novel immunotherapeutic strategies to restore immune control and reduce disease recurrence in JORRP patients. - Source: PubMed
Publication date: 2026/06/02
Li ShilanWang WeiPeng YunWang GuixiangXi YueWang ShengcaiZhao JingZhang FengzhenWang HuaLi HongbinDuan QingchuanLong TingGui JingangNi XinZhang Jie - Tacrolimus (TAC), a widely used immunosuppressive agent, is associated with significant nephrotoxicity characterized by renal inflammation and fibrosis. Simvastatin (SIM), beyond its lipid-lowering effects, exhibits pleiotropic anti-inflammatory and anti-fibrotic properties. This study aimed to explore the protective effect of SIM against TAC-induced renal injury, with a focus on the potential involvement of the CXCL16/ADAM10 signaling axis. Adult male Wistar rats were divided into four groups (n = 10 per group): control, SIM-treated (SIM; 10 mg/kg/day), TAC-treated (TAC; 2 mg/kg/day), and SIM + TAC-treated. All medications were given orally for 28 days. Hematological indices, renal function parameters, and lipid profile were assessed. Histopathological evaluation and immunofluorescence analysis of CXCL16, ADAM10, fibronectin and TGF-β were performed. TAC administration resulted in significant renal dysfunction, dyslipidemia, and marked histopathological alterations, accompanied by upregulation of CXCL16, ADAM10, and fibrotic markers. Conversely, co-administration of SIM and TAC improved renal function, attenuated lipid abnormalities, and preserved renal architecture. These effects were associated with decreased the expression of CXCL16, ADAM10, TGF-β and fibronectin. SIM demonstrates significant kidney-protective properties against TAC-induced renal injury, potentially involving modulation of the CXCL16/ADAM10 signaling pathway. These findings indicate that SIM could be a beneficial supplementary treatment to alleviate the serious kidney-damaging effects associated with TAC. - Source: PubMed
Publication date: 2026/05/29
Alelowi Abdulrahman AAlradhi AluluAlhowail Ahmad HAldubayan Maha AAbdel-Bakky Mohamed S - Extracellular vesicles (EVs) are naturally occurring nanoparticles secreted by diverse cell types and are increasingly explored as delivery vehicles and immunomodulatory platforms. Rigorous preclinical safety and immunotoxicological evaluation is therefore essential prior to clinical translation. Here, using a modified OECD 423 acute toxicity class method, we assessed the toxicity of EVs loaded with glucose oxidase (GOX) along with T-dependent antibody response (TDAR) analyses in repeated-dose toxicity studies. - Source: PubMed
Publication date: 2026/05/11
Grudzinski Ireneusz PBamburowicz-Klimkowska MagdalenaSochanowicz BarbaraBrzoska KamilProchorec-Sobieszek MonikaCabaj MarzenaTargonska AlicjaStawarska AgnieszkaKruszewski Marcin