Ask about this productRelated genes to: TL1A protein
- Gene:
- TNFSF15 NIH gene
- Name:
- TNF superfamily member 15
- Previous symbol:
- -
- Synonyms:
- TL1, VEGI, TL1A, VEGI192A, MGC129934, MGC129935
- Chromosome:
- 9q32
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2017-03-02
Related products to: TL1A protein
Related articles to: TL1A protein
- Asthma remains a global health burden, with its heterogeneity necessitating precision biomarkers and targeted therapies. Tumor necrosis factor-like ligand 1A (TL1A), a novel alarmin in the airway, remains poorly characterized in asthma pathogenesis. TL1A levels were measured in the sputum and serum samples of patients with various asthma phenotypes. Single-cell RNA sequencing of murine asthmatic lung and myeloid-cell-specific -knockout mice ( ) was performed, and the effects of anti-TL1A interventions were evaluated in allergen-induced asthma models. TL1A levels were significantly elevated in the serum and sputum of patients with asthma and correlated with clinical disease severity, declining lung function, and blood eosinophil counts. Single-cell RNA sequencing identified macrophages as the primary immune cells expressing TL1A in the context of allergic lung inflammation. In the mice, allergen-induced airway inflammation, T helper 2 cytokine secretion, and mucus hypersecretion were attenuated. Mechanistically, TL1A induced C-C motif chemokine ligand 8 (CCL8) expression via the activation of death receptor 3, thereby driving type 2 inflammation. Critically, the anti-TL1A antibody interventions suppressed T helper 2-mediated responses and reduced the number of pathogenic CD8 T cells in a dose-dependent manner. TL1A serves a dual role as a biomarker and therapeutic target in asthma, as it modulates macrophage-driven pathogenesis. TL1A inhibition disrupts CCL8/C-C motif chemokine receptor 8 signaling and pathogenic T-cell responses, providing a precision medicine strategy for asthma. - Source: PubMed
Publication date: 2026/04/09
Zhang JintaoLiu XiaofeiQi QianPan YunZeng RongQiao ChenxiaoXu ChangjuanWang PengfeiShi ShuochuanWang YingLiu XueminDong Liang - Epithelial-mesenchymal transition (EMT) plays a critical role in tumor progression; however, the underlying molecular mechanisms of EMT in papillary thyroid carcinoma (PTC) remain incompletely understood. This study aimed to investigate EMT-related mechanisms in PTC using an integrative approach combining single-cell RNA sequencing and machine learning. - Source: PubMed
Xu TianfengSun RuonanZhang YujieZheng Xun - Tumor Necrosis Factor (TNF)-like cytokine 1A (TL1A) is a member of the TNFSF superfamily, with the ability to associate to Death Domain Receptor 3 (DR3) but also to Decoy Receptor 3 (DcR3). Functional signaling affects several DR3-bearing cells and critically regulates diverse immunological processes such as adaptive lymphocytic responses, homeostatic mucosal pathways, as well as fibrotic mechanisms. The multifaceted pleiotropic nature of the TL1A/DR3 system appears to be critically involved in the pathogenesis of inflammatory and autoimmune diseases, particularly Inflammatory Bowel Disease (IBD) and allergic lung inflammation and may represent a novel therapeutic target for patients. In fact, several clinical programs with anti-TL1A monoclonal antibodies are currently underway and initial results from clinical trials in patients with IBD report positive effects on clinical and endoscopical outcomes with favorable safety profile. In this narrative review, we aim to link the immunological characteristics of the TL1A/DR3 cytokine: receptor system with the pathogenesis of IBD but also other immune-mediated conditions by critically revisiting mechanistic evidence from animal models and associations with human disease states. We also review available information on the use of anti-TL1A monoclonal antibodies and comment on future challenges that may be associated with the therapeutic potential of targeting the TL1A/DR3 pathway. - Source: PubMed
Publication date: 2026/01/23
Kitsou KonstantinaKokkotis GeorgiosBamias Giorgos - This work conducted a transcriptome analysis of canine intestinal epithelial cells (cIECs) treated with nicotinamide mononucleotide (NMN), a physiologically active nucleotide with a pyridine base known for its anti-aging and anti-inflammatory effects. In our experiment, cIECs were cultured and segregated into a control group (Ctrl) and an NMN-treated group. The finding demonstrated that NMN significantly affects cell proliferation in cIECs in comparison to the Ctrl. The transcriptome analysis indicated a high enrichment of genes associated with the cell cycle, proliferation, cellular senescence, and inflammatory pathways in NMN-treated cIECs, showing that NMN has the capacity to modify these biological processes. Compared to the Ctrl group, NMN treatment significantly increased ATP, SOD, CAT and GSH levels and decreased the activities of ROS and MDA. NMN treatment also significantly increased the activity of the relative complex I, III and V enzymes compared to the Ctrl group. Furthermore, the expression of , , , and were decreased significantly, while , , and were increased significantly in NMN-5μM treatment compared to Ctrl. NMN-treated significantly decreased the expression of , and , while increasing the expression of Kdm5a, Kdm5b and Kdm5c compared to the Ctrl group. Additionally, ChIP-qPCR use discovered that NMN-treatment significantly downregulated the enrichment of EDN-1 at target loci of , , , and compared to the Ctrl group. Expression of the gene suggests that its exert in biological activities by inhibiting inflammatory responses and anti-aging pathways. Then, we detected the transcriptional activation linked histone markers and found that and were significantly downregulated, while was significantly upregulated in the NMN-treatment compared to the Ctrl group. We conclude that NMN regulates EDN-1 expression in cIECs through mechanisms involving NR4A1 and histone modifications, highlighting its potential role in canine intestinal health. - Source: PubMed
Publication date: 2026/02/13
Guo XudongZhu ChuyangAdam Saber YZhu CuipengLiu Hao-YuCai Demin - Adipogenesis, the intricate process of differentiation from preadipocytes or mesenchymal stem cells into mature adipocytes, is crucial for the formation and metabolic function of adipose tissues in mammals. The TNF ligand-related molecule 1A (TL1A) is a type II transmembrane protein belonging to the TNF superfamily. Inflammation is involved in the whole process of adipocyte cell formation and obesity development. To investigate the potential influence of TL1A on adipocyte development, we examined mouse embryo fibroblasts (MEFs) and 3T3-L1 cells. Our findings indicated that TL1A-treated MEFs exhibited an elevated rate of spontaneous adipogenesis, with a significant enhancement in adipocyte formation upon induction with a combination of insulin, dexamethasone and methylisobutylxanthine. This increased adipogenesis was evidenced by augmented lipid droplet formation and elevated expression of several adipogenic markers. Specifically, there was an upregulation of early-stage adipogenesis genes, including Krox20, KLF5, C/EBPβ and C/EBPδ, as well as late-stage adipogenesis regulators such as KLF15, C/EBPα, PPARγ and aP2. Moreover, TL1A significantly upregulated the protein expression of adipogenic markers (C/EBPα, C/EBPβ, PPARγ, CD36 and aP2) in MEFs and 3T3-L1 cells. Mechanistically, TL1A enhanced the phosphorylation of yes-associated protein 1 (YAP1), which led to cytoplasmic retention. Ultimately, TL1A inhibited the stabilization and nuclear transfer of β-catenin in MEFs, probably through regulating the upstream protein YAP1. Taken together, TL1A promoted adipogenic differentiation of MEFs and 3T3-L1 cells in vitro, which partly via inhibiting YAP1 mediated β-catenin signaling pathway. - Source: PubMed
Publication date: 2026/02/19
Chang ZiqiWang QiaoyuZhai YanLi KeZheng XianjieWang YaohuiZhao Dan