AITRL, Human Recombinant proteins
- Known as:
- AITRL, Human Recombinant proteins
- Catalog number:
- 7113-10
- Product Quantity:
- 10 μg
- Category:
- Proteins
- Supplier:
- Biovis
- Gene target:
- AITRL Human Recombinant proteins
Related genes to: AITRL, Human Recombinant proteins
- Gene:
- TNFSF18 NIH gene
- Name:
- TNF superfamily member 18
- Previous symbol:
- -
- Synonyms:
- AITRL, TL6, hGITRL
- Chromosome:
- 1q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-15
- Date modifiied:
- 2017-03-02
Related products to: AITRL, Human Recombinant proteins
Related articles to: AITRL, Human Recombinant proteins
- Background Although infection is a primary risk factor for gastric cancer (GC), the specific bacterial components that causally drive carcinogenesis remain poorly understood. Traditional epidemiological studies are limited by confounding variables and the potential for reverse causation. This study aimed to dissect the causal effects of host antibody responses to various antigens on GC risk using Mendelian randomization (MR). Methodology We conducted a two-sample MR study using summary statistics from large-scale genome-wide association studies (GWAS) of European-ancestry populations. Genetic instruments were selected for general seropositivity and antibody levels against six antigens: cytotoxin-associated gene A (CagA), Catalase, GroEL, outer membrane protein (OMP), urease subunit A (UreA), and vacuolating cytotoxin A (VacA). The primary outcome was GC. Inverse-variance weighted (IVW) MR served as the main analysis, with comprehensive sensitivity analyses to assess the robustness of results. Multivariable MR (MVMR) was used to estimate the direct effects of each serotype, and a two-step mediation analysis was performed to explore potential mediating pathways. Results Genetically predicted general seropositivity was causally associated with an increased risk of GC (odds ratio (OR): 1.12, 95% confidence interval (CI): 1.01-1.24; = 0.027). The host antibody response to OMP showed a stronger causal effect (OR: 1.19, 95% CI: 1.08-1.30; < 0.001). In contrast, no causal effects were observed for antibody responses to the classic virulence factors CagA or VacA ( > 0.05). In multivariable analysis, the effect of the anti-OMP response remained robust (OR: 1.18, 95% CI: 1.07-1.30; = 0.001), while the association for general seropositivity was attenuated to null. Mediation analysis implicated tumor necrosis factor ligand superfamily member 18 (TNFSF18) as a potential mediator of the -GC pathway, accounting for a substantial portion of the total effect (estimated at 47.0%), though this finding did not reach statistical significance (= 0.077). Conclusions This MR study provides genetic evidence that the host immune response to OMPs, rather than to classic virulence factors like CagA, is a key contributor to gastric carcinogenesis. This effect appears to be partially mediated by the inflammatory TNFSF18 pathway, suggesting that the chronic host-bacterial interactions at the gastric epithelial surface are critical to malignant transformation. - Source: PubMed
Publication date: 2025/07/31
Rao WentaoXue ChenghongGan DonghuiLiu Binjian - In this study, we investigated PSD3, CD274 (PD-L1), and TNFSF18 as potential immune-related biomarkers in esophageal squamous cell carcinoma (ESCC) using integrative transcriptomic and experimental approaches. CD274 and TNFSF18 were consistently up-regulated in ESCC across both TCGA and GEO datasets, while PSD3 showed significantly higher expression in TCGA but no significant difference in the GEO cohort. Only PSD3 demonstrated a significant association with overall survival, with higher expression correlating with improved prognosis. Interestingly, despite its favorable prognostic value, PSD3 functionally promoted ESCC cell proliferation, invasion, and migration , while inversely regulating PD-L1 expression. Conversely, heterozygous knockout of PD-L1 in KYSE150 cells impaired tumor aggressiveness. Co-immunoprecipitation revealed a direct physical interaction between PSD3 and PD-L1, suggesting a regulatory axis with implications for immune evasion. These findings position PSD3 as a context-dependent immuno-oncogenic factor and a potential therapeutic target in ESCC. - Source: PubMed
Publication date: 2025/08/15
Luo ShujuanLi HuifangCai BangwuNurbahati AididarCui HongPeng TianyuanWang WeiLiu QingLu XiaomeiZheng Shutao - Esophageal cancer (EC) ranks among the most prevalent malignancies globally and represents a significant and growing public health burden. This study aimed to construct a prognostic model leveraging anoikis-related genes (ARGs) to predict patient survival and elucidate the immunological microenvironment in EC. The findings are anticipated to enhance prognostic accuracy and inform therapeutic strategies, ultimately improving patient outcomes and treatment efficacy. - Source: PubMed
Publication date: 2025/07/11
Su YaniZhang MingXu PengWen PengfeiXu KeXie JialeWan XianjieLiu LinYang ZhiYang Mingyi - We investigated the effects of maternal vitamin and mineral supplementation throughout gestation on gene expression in the jejunal mucosa of neonatal calves. Crossbred Angus heifers ( = 14) were estrus synchronized, bred to female-sexed semen, and randomly assigned to a basal diet (Control, CON; = 7) or the basal diet plus vitamin and mineral supplement (Treatment, VTM; = 7). After parturition, calves were removed from their dams before suckling, fed colostrum replacer, and euthanized 30 h after the first feeding. A subsample of the mucosa of the mid-jejunum was collected, and total RNA was isolated. Gene expression was measured using RNA-Seq, and differentially expressed genes (DEGs) were identified using DESeq2. We identified 528 DEGs from the jejunal mucosa between the VTM and CON calves ( ≤ 0.05 and |log2FC| ≥ 0.5). The DEGs were associated with nutrient transport, lipid metabolism, and immune-related biological processes and pathways. Interestingly, genes underlying the complement and coagulation cascades were mostly downregulated in calves born to VTM dams. On the other hand, the cytokine-cytokine receptor interaction KEGG pathway showed most genes upregulated ( and ). Our results show that vitamin and mineral supplementation throughout gestation affects genes underlying tissue structure, nutrient transport and metabolism, and immune system pathways in neonates. The implications of such changes and the long-term outcomes on herd health and performance warrant further research. - Source: PubMed
Publication date: 2025/06/26
Craner Audrey JDahlen Carl RHurlbert Jennifer LMenezes Ana Clara BBanerjee PriyankaBaumgaertner FriederikeBochantin-Winders Kerri AAmat SamatSedivec Kevin KSwanson Kendall CDiniz Wellison J S - The insufficient activation, infiltration, and functional suppression of tumor-killing cells in the tumor microenvironment (TME) collectively hinder antitumor immunity. CCR7, CXCL16, and GITRL are well-established immune modulators with potential to enhance immunotherapy efficacy. Herein, we developed lipid nanoparticle-encapsulated mRNA (LNP-mRNA) encoding these three targets with the aim of enhancing dendritic cell (DC) immunogenicity and improving the immunosuppressive TME. DCs were stimulated in vitro with LNP-mRNA to evaluate its effects on DC function. The systemic immune response of LNP-mRNA was characterized. To assess the antitumor effect of LNP-mRNA, B16-OVA tumor-bearing mouse models were constructed. Humanized Raji-engrafted mouse models were constructed to investigate the synergistic effect of LNP-mRNA and anti-PD-1 antibody. Results demonstrated that LNP-mRNA enhanced the function of DCs. Furthermore, LNP-mRNA promoted T cell activation and effector differentiation while suppressing regulatory T cell infiltration. Intratumoral administration of LNP-mRNA elicited potent immune response and induced regression of established tumors. In humanized Raji-engrafted mouse models, the combination use of LNP-mRNA and anti-PD-1 antibody synergistically amplified antitumor immunity. Overall, our research demonstrates that the synthesized LNP-mRNA enables durable tumor control through coordinated enhancement of DC functionality, T cell priming, and immunosuppressive TME remodeling. This multi-functional strategy marks a transformative advancement in tumor immunotherapy. - Source: PubMed
Publication date: 2025/05/30
Chen JianyuCen QingyanHu RongQiu YingqiZhang HonghaoWang HaoHu YuxingXie XiaolingLi Yuhua