Ask about this productRelated genes to: CCL16 antibody
- Gene:
- CCL16 NIH gene
- Name:
- C-C motif chemokine ligand 16
- Previous symbol:
- SCYA16
- Synonyms:
- NCC-4, SCYL4, LEC, HCC-4, LMC, LCC-1, CKb12, Mtn-1
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-11
- Date modifiied:
- 2016-03-01
Related products to: CCL16 antibody
Related articles to: CCL16 antibody
- Compare cold adaptation mechanisms between cold-tolerant Hezuo and cold-sensitive Bama pigs. - Source: PubMed
Publication date: 2026/03/11
Li YajuanGao XiaoliZhang YatingGun Shuangbao - The escalating annual death toll attributed to Cholangiocarcinoma (CCA) is, in part, a consequence of delayed diagnosis. This study developed an optimal CCA diagnostic model through the application of 11 machine-learning algorithms. Initially, 105 differentially expressed genes (DEGs) were identified by analyzing gene expression profiles from 307 CCA tumor tissues and 124 adjacent non-tumor tissues. WGCNA, F-test, characteristic importance, and Lasso regression analysis were employed to identify key DEGs, including APOF, DIO1, APOM, and OTC. Subsequently, diagnostic models were constructed based on APOF, DIO1, and OTC using 11 machine-learning algorithms. The LightGBM algorithm was determined as the optimal model through ROC curve analysis and machine learning performance evaluation, achieving an AUC of 0.84, with accuracy, precision, and recall values of 0.80, 0.83, and 0.90, respectively. Subsequent analyses included gene enrichment, protein-protein interaction (PPI), and CCA-related drug assessments. Additionally, the study revealed an imbalance in immune cell infiltration in CCA and identified CCL16 as a chemokine involved in immunoregulation. RT-qPCR confirmed that APOF, DIO1, and OTC were significantly downregulated in CCA tumor tissues. In conclusion, this research provides new directions for the diagnosis and immunotherapy of this disease. - Source: PubMed
Publication date: 2025/12/02
Zhang ZeyuGeng XueyanYin MaopengLiang YongyuanZheng Guixi - Hepatocellular carcinoma (HCC) is characterized by aberrant tumor vasculature and an immunosuppressive tumor microenvironment (TME), both of which compromise immunotherapy efficacy while promoting circulating tumor cell (CTC) dissemination and immune escape. In this study, we aimed to identify potential therapeutic targets for remodeling aberrant tumor vasculature by analyzing CTCs from patients with early-stage HCC. HCC tissue samples derived from patients with elevated CTC counts demonstrated significant CCL16 downregulation accompanied by vascular structural abnormalities and an immunosuppressive TME. CCL16 deficiency in murine models exacerbated both vascular dysfunction and immunosuppressive TME formation, whereas CCL16 overexpression mediated vascular normalization and promoted immune cell infiltration. Mechanistically, CCL16 interacted with ICAM-1 receptor on tumor-associated macrophages, triggering JAK2-STAT6 pathway activation and subsequent IL24 secretion. Pharmacologic intervention using sitagliptin, a DPP4 inhibitor, effectively stabilized tumor vasculature by preventing CCL16 degradation. Importantly, therapeutically elevating CCL16 levels combined with anti-PD-1 antibody administration synergistically enhanced vascular normalization and improved antitumor immunity in HCC models, suppressing tumor growth. These findings establish CCL16 as a critical regulator of vascular-immune cross-talk and propose DPP4 inhibition as a promising therapeutic strategy for treating HCC. - Source: PubMed
Chen KunlingFeng HuolunZhang YujiePei JingyuanXu YuyanWei XiangxuChen ZhuohaoFeng ZhoubinCai LeiLi YongZhao LiangPan Mingxin - The aim of this study was to investigate the changes in the gut microbiota and proteins related to metabolism and immunity caused by childhood obesity and insulin resistance (IR) and to assess the underlying relationship between the gut microbiota and IR in children. Nineteen children with obesity and sixteen healthy children were recruited. Children with obesity were divided into two groups: obese with IR and obese without IR. All of the obese children participated in a 1-month lifestyle-based weight loss program. Faecal metagenomics and serum Olink proteomics combined with clinical parameters were used to identify the metabolic alterations associated with childhood obesity and IR. The gut microbiota and serum protein were significantly altered in obese children with IR. The relative abundances of Akkermansia muciniphila, IGFBP1 and GP6 were decreased in obese children with IR. Butyricicoccus sp. AM29-23AC, DLK1, CD163, CCL16 and CTSD levels were recovered after IR improved. TNFR1 had a significant indirect effect on the interaction between s-Citrobacter.freundii and fasting insulin. In conclusion, obese children with IR have abnormal gut microbiota and serum proteins related to metabolism and immunity, which can be improved after weight loss. The gut microbiome of children with obesity may contribute to the development of IR by triggering metabolic inflammation.Clinical Trial Registration: This study was registered with the Chinese Clinical Trial Registry (Registration number: ChiCTR2300072179). - Source: PubMed
Publication date: 2025/07/01
Liu LujieLi MengQin YujieLiu YueshengLi MinLian BiyaoGuo RuilongXiao YanfengYin Chunyan - Genetic polymorphisms have been linked to the differential waning of vaccine-induced immunity against COVID-19 following vaccination. Despite this, evidence on the mechanisms behind this waning and its implications for vaccination policy remains limited. We hypothesize that specific gene variants may modulate the development of vaccine-initiated immunity, leading to impaired immune function. This study investigates genetic determinants influencing the sustainability of immunity post-mRNA vaccination through a genome-wide association study (GWAS). Utilizing a hospital-based, test negative case-control design, we enrolled 1,119 participants from the Taiwan Precision Medicine Initiative (TPMI) cohort, all of whom completed a full mRNA COVID-19 vaccination regimen and underwent PCR testing during the Omicron outbreak. Participants were classified into breakthrough and protected groups based on PCR results. Genetic samples were analyzed using SNP arrays with rigorous quality control. Cox regression identified significant single nucleotide polymorphisms (SNPs) associated with breakthrough infections, affecting 743 genes involved in processes such as antigenic protein translation, B cell activation, and T cell function. Key genes identified include CD247, TRPV1, MYH9, CCL16, and RPTOR, which are vital for immune responses. Polygenic risk score (PRS) analysis revealed that individuals with higher PRS are at greater risk of breakthrough infections post-vaccination, demonstrating a high predictability (AUC = 0.787) in validating population. This finding confirms the significant influence of genetic variations on the durability of immune responses and vaccine effectiveness. This study highlights the importance of considering genetic polymorphisms in evaluating vaccine-induced immunity and proposes potential personalized vaccination strategies by tailoring regimens to individual genetic profiles. - Source: PubMed
Publication date: 2024/09/10
Hsieh Min-JiaTsai Ping-HsingChiang Pin-HsuanKao Zih-KaiZhuang Zi-QingHsieh Ai-RuHo Hsiang-LingChiou Shih-HwaLiang Kung-HaoChen Yu-Chun