TNFSF18
- Known as:
- TNFSF18
- Catalog number:
- AP30365PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- TNFSF18
Related genes to: TNFSF18
- 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: TNFSF18
Activation-inducible TNF-related ligand,AITRL,AITRL,GITRL,Glucocorticoid-induced TNF-related ligand,hGITRL,Homo sapiens,Human,TL6,TNFSF18,Tumor necrosis factor ligand superfamily member 18,UNQ149_PRO1AITRL Anti-Human Host: Rabbit TNFSF18; TL6; AITRL; GITRL; hGITRLAITRL , Host: Rabbit, Species: Anti-Human, Synonyms: TNFSF18; TL6; AITRL; GITRL; hGITRLAITRL Human Host: E. coli TNFSF18; TL6; AITRL; GITRL; hGITRLAITRL, Host: E. coli, Species: Human, Synonyms: TNFSF18; TL6; AITRL; GITRL; hGITRLanti-TNFSF18anti-TNFSF18anti-TNFSF18anti-TNFSF18anti-TNFSF18anti-TNFSF18anti-TNFSF18 (6F7)anti-TNFSF18 (6F7)anti-TNFSF18 type: Primary antibodies host: Mouseanti-TNFSF18 type: Primary antibodies host: Rabbit Related articles to: TNFSF18
- Prostate cancer (PCa) is prototypically immunologically "cold", characterized by low tumor mutational burden, sparse CD8 T-cell infiltration, and resistance to immune checkpoint blockade. The tumor cell-intrinsic programs driving immune evasion in this context remain incompletely defined. - Source: PubMed
Publication date: 2026/03/18
Liu WeihaoLi GuopingLei YanLiu HuixiuWang BinhuiDeng WeimingHong YudeLong Xiangyang - The hostile tumor microenvironment (TME) remains a major challenge for cancer immunotherapy. In this study, we performed TME-targeted in vivo CRISPR activation (CRISPRa) screen to identify factors that promote antitumor immunity, culminating in rationally designed immune gene therapy combinations. Multiplexed activation of genes encoding antigen presentation, T-cell proliferation, costimulation, and migration (APCM) leads to enhanced antitumor responses. An APCM-focused CRISPRa screen in metastatic tumors identified Cd80, Tnfsf14, Cxcl10, Tnfsf18, Tnfsf9, and Ifng as top immunostimulatory candidates. Further optimization pinpointed Tnfsf9 (4-1BBL) + Ifng + Il12b (4II) as a potent therapeutic combination. Adeno-associated virus (AAV) 4II enhanced antigen presentation, T-cell activation, proliferation, cytotoxicity, and tumor infiltration. Preconditioning the TME with AAV-4II synergized with chimeric antigen receptor (CAR) and T-cell receptor (TCR) T-cell therapies to suppress primary and metastatic solid tumors in vivo. These findings establish TME-targeted CRISPRa screening as a rapid route to develop immune gene therapy combinations against solid tumors. - Source: PubMed
Zhang FeifeiDong ChuanpengChow Ryan DXin ShanHe EmilyFeng YanzhiZhu LvyunMirza DaniyalTian XiaolongYang LuojiaZhou LiqunLing XinyuHan QinFan RongChen SidiWang Guangchuan - Immune checkpoint regulators can improve neurological functions in Alzheimer's disease. However, it remains blurred whether these regulators may ameliorate temporal lobe epilepsy (TLE) and TLE-related cognitive impairment. This study analyzed the bulk transcriptomic data of human TLE hippocampi by bioinformatics. The expression of the potential immune checkpoint regulators in the hippocampus was assessed by immunohistochemical staining; the preoperative seizure severity and postoperative cognitive function were evaluated by the National Hospital Seizure Severity Scale (NHS3) and Telephone Interview for Cognitive Status-Modified (TICS-m); the correlation between the target immune checkpoint regulators and TLE-related cognitive impairment was examined by simple linear regression models and the area under the receiver operating characteristic curve (AUC). We first identified glucocorticoid-induced tumor necrosis factor receptor ligand (GITRL) as a key immune checkpoint regulator in TLE patients, with an increased intensity of GITRL in epileptic hippocampus (n = 21) compared with that of the control (n = 3). The GITRL intensity was positively correlated with NHS3 score (r = 0.503, p < 0.001) and negatively with TICS-m total score (r = 0.456, p < 0.001), specifically, TICS-m memory score (r = 0.360, p = 0.004), TICS-m language/attention score (r = 0.319, p = 0.008), and TICS-m orientation score (r = 0.312, p = 0.008). The AUC showed that the GITRL intensity presented a good predictive performance in discerning patients with a TICS-m score of ≥ 30 (AUC: 0.875, 95% CI, 0.721-1.00; p = 0.013). These findings highlight hippocampal GITRL as a potential predictive marker for TLE-related cognitive impairment. - Source: PubMed
Li ManShi JinyingPan XiaodongHuang Huapin - The prevalence of autoimmune diseases such as inflammatory bowel disease (IBD) and rheumatoid arthritis (RA) is increasing. Glucocorticoid-induced TNFR-related protein (GITR), a TNF receptor superfamily (TNFRSF) member, is activated by GITR-ligand (GITRL). GITR signaling is pathogenic in models of RA and IBD, leading to lymphocyte proliferation and secretion of pro-inflammatory cytokines. Despite promising preclinical data, GITR neutralization in autoimmune diseases remains under-explored, due to challenges in avoiding antibody-mediated GITR activation. Therefore, we developed a human GITR-specific antibody that inhibits GITRL-mediated GITR-signaling, while preserving the GITRL epitope on GITR. The antibody strongly inhibited GITR signaling in the in vitro assays via a novel mechanism of disrupting downstream higher-order structures rather than direct blocking of GITR binding. Even though the antibody did not demonstrate efficacy in an NSG human skin graft transplant model, this general mechanism might be a viable therapeutic intervention for other TNFRSF members relying more significantly on soluble ligands. - Source: PubMed
Publication date: 2025/12/18
Yan JingMin-DeBartolo JessicaHuang Ching-ShinSharif M NusratLi LiFish SusanDower CoreyMurphy DeniseAndreyeva TatyanaLiu HengHan XinbingZheng WeiOoi Jot HuiEdmonds JasonChen TingMaben ZacharyStevens Chad RGoihberg PolinaNocula-Lugowska MalgorzataEvans Steven MMosyak LidiaKelleher KerryDickinson CaitlynHegen MartinWinkler AaronKarlsson Fridrik - Rabies, a zoonotic infectious disease causing central nervous system inflammation, remains a threat to public health in regions with limited medical resources. Vaccination effectively reduces rabies incidence and mortality, underscoring the need for vaccines that are cost-effective, immunogenic, protective, and safe. This study constructed a recombinant rabies virus (rRABV)-overexpressing glucocorticoid-induced tumor necrosis factor receptor ligand (GitrL), named rLBNSE-GitrL, using a reverse genetic operating system. rLBNSE-GitrL exhibited similar in vitro phenotypic characteristics and immune safety as the parent RABV (rLBNSE). This recombinant virus stimulated the production of a greater number of activated dendritic cells (DCs) compared to rLBNSE. The enhanced innate immune response induced by rLBNSE-GitrL may be mediated through the activation of innate immune-related signaling pathways, such as the tumor necrosis factor (TNF), and chemokine signaling pathways, and the upregulation of a series of innate immune-related genes, including MMP2, IL-6, CXCL9, TIMP1, IL-17d, and TNF-α. Consequently, rLBNSE-GitrL elicited significantly higher levels of RABV vaccine-induced virus-neutralizing antibodies (VNA), IgG, and IgM compared to rLBNSE as early as 3 days post-immunization (dpi), thereby improving the protective effect in mice. Collectively, the overexpression of GitrL facilitated the induction of early and potent antibody responses following RABV immunization. - Source: PubMed
Publication date: 2025/10/09
Wang YufangXing XiaoXiong ZhiminWang YongLiu YapingLi Yingying