TNFSF18
- Known as:
- TNFSF18
- Catalog number:
- SM2258P
- Product Quantity:
- 0.25 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
- Regulatory T cells play a pivotal role in shaping immune interactions, limiting antitumor immunity, and impairing the activity of engineered effector cells. Overcoming regulatory T (Treg) cell-mediated immunosuppression is critical to unlock the full therapeutic potential of chimeric antigen receptor (CAR)-cell therapies. Here, we develop "armored" anti-CD19 CAR-NK cells coexpressing GITR ligand (GITRL) (CAR19-GITRL-NK) to both target malignant B cells and locally counteract Treg-mediated suppression. GITR is highly expressed on Tregs, and engagement by its ligand GITRL can modulate their function, providing a rational strategy to reprogram the tumor microenvironment. - Source: PubMed
Publication date: 2026/07/07
Schmidt DayaneEbrahimabadi SimaTirapelle Mariane CariatiGarcia Ferreira Camilly MeloDos Santos Matheus HenriqueBiggi Alison Felipeda Silva Januário Mara ElisamaCalado Rodrigo TocantinsPicanço-Castro Virginia - Anaplastic thyroid carcinoma (ATC) may arise from the progression of differentiated thyroid cancers, but the mechanisms are not well understood. Establishing appropriate animal models and conducting ultrasound imaging monitoring can facilitate the study of this dedifferentiation process. - Source: PubMed
Publication date: 2026/06/28
Jin AnqiWang ShiyuWang JianYu PengchengWang YulongShi JunZhou Shichong - 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