Ask about this productRelated genes to: TNFSF18 protein
- 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 protein
Related articles to: TNFSF18 protein
- 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. Here, we performed TME-targeted in vivo CRISPR activation (CRISPRa) screen to identify factors that promote anti-tumor immunity, culminating in rationally designed immune gene therapy combinations. Multiplexed activation of genes encoding antigen presentation, T cell proliferation, co-stimulation, and migration (APCM) leads to enhanced anti-tumor 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. AAV-4II enhanced antigen presentation, T cell activation, proliferation, cytotoxicity, and tumor infiltration. Preconditioning the TME with AAV-4II synergized with CAR-T and 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
Publication date: 2026/02/27
Zhang FeifeiDong ChuanpengChow Ryan DXin ShanHe EmilyFeng YanzhiZhu LvyunMirza DaniyalTian XiaolongYang LuojiaZhou LiqunLing XinyuHan QinFan RongChen SidiWang Guangchuan - 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 - - Source: PubMed
Publication date: 2025/10/07
Zhang DongdongZhang PeiJing RanChen ZiweiCai Ming