L4G9 TL1A
- Known as:
- L4G9 TL1A
- Catalog number:
- mc-577
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- L4G9 TL1A
Related genes to: L4G9 TL1A
- 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: L4G9 TL1A
Related articles to: L4G9 TL1A
- Diminished lymphocyte infiltration and activation in ovarian cancer are attributable to the malignancy and irresponsiveness to immunotherapy. We show here that treatment of a murine model of ovarian cancer with recombinant tumor necrosis factor superfamily-15 (TNFSF15) results in a marked inhibition of peritoneal dissemination of the cancer cells and a substantial reduction of ascites. The treatment leads to normalization of the tumor vasculature judged by enhanced coverage of the neo-blood vessels with PDGFβ pericytes and diminished levels of the hypoxia-responsive cancer stem cell marker CD133. Additionally, the treatment gives rise to accumulation of Lyve-1 lymphatic endothelial cells and PNAd high endothelial venules (HEV) in the tumors, consistent with the formation of tertiary lymphoid structures (TLS). Moreover, the treatment results in facilitated tumor infiltration of T cells, B cells, macrophages, and dendritic cells, the latter exhibit upregulated expression of TLS-associated cytokines and chemokines, including Lt-α, Lt-β, IFN-β, TNF-α, CCL19, CCL21, CXCL13, and CXCL10. Furthermore, there is an enhanced responsiveness in TNFSF15-treated tumors toward PD-1 blockade treatment. These findings suggest that TNFSF15 is capable of facilitating vascular normalization and TLS formation, and thus promoting a reinstitution of the immune microenvironment in ovarian cancer. - Source: PubMed
Wang Jing-YingWang Yu-YingZhang Li-SongWeng Shi-TingCui Hai-YanZhang Zhi-SongLi Lu-Yuan - Despite major therapeutic advances, many patients with inflammatory bowel disease (IBD) continue to experience inadequate treatment response, progressive disease, and irreversible complications requiring surgery. Current management is constrained by a biological efficacy ceiling and lack of agents directly targeting key drivers of fibrosis and barrier dysfunction. This systematic review synthesizes current knowledge on tumor necrosis factor-like cytokine 1A (TL1A) and death-domain receptor 3 (DR3) signaling pathways, critically evaluates the therapeutic potential of TL1A-targeted interventions, and explores future directions for precision medicine applications in IBD care. - Source: PubMed
Liang Raymond Fueng-HinPugliano Cecilia LinaHughes RobertMajumder SnehaliLo Bello AntonioIacucci MariettaGhosh Subrata - TL1A is a proinflammatory cytokine in the tumor necrosis factor (TNF) superfamily that signals via DR3 on T helper cells, innate lymphoid cells, and fibroblasts. Dysregulated TL1A signaling has been hypothesized to affect multiple immune-mediated diseases, with clinical proof of concept demonstrated in ulcerative colitis and Crohn's disease. We characterized the binding affinity, specificity, structure, pharmacodynamics, pharmacokinetics, and toxicity profiles of SPY002 and SPY072, two novel extended half-life monoclonal antibodies that inhibit TL1A. SPY002 and SPY072 demonstrated selective, high-affinity binding to human TL1A (K ≈ 31-35 pM) and potent functional inhibition of DR3 signaling. Based on Fc modifications, SPY002 and SPY072 showed attenuated Fc effector function and increased FcRn binding at acidic pH (5.8). Both antibodies exhibited enhanced PK profiles in nonhuman primates, resulting in predicted human half-lives that support quarterly or biannual dosing. In toxicity studies, no drug-related adverse effects were observed with either antibody at exposures >10 times those anticipated in clinical trials. In a rat collagen-induced arthritis model, anti-TL1A antibody treatment effectively reduced arthritis severity, with similar efficacy to the TNF antagonist etanercept. In humanized mouse Imiquimod-induced psoriasis and 2,4,6‑trinitrobenzene sulfonic acid colitis models, anti-TL1A demonstrated similar efficacy to anti-IL-23 and anti-TNF antibodies. These findings characterize two novel extended half-life TL1A antibodies and support the ongoing Phase 2 clinical development of SPY002 and SPY072 for immune-mediated diseases such as inflammatory bowel disease and rheumatic diseases. - Source: PubMed
Publication date: 2026/05/10
Siegel MatthewZhu EricRios DanielKang Byong HMcNally JustinKennedy MichaelHew KinjalPatel PreeyamBallew OliviaGiles David HLewis Emily M ALaFountaine JustinOh JasonFriedman Joshua RRose Mark JShaheen HussamSpencer Andrew G - Hidradenitis suppurativa (HS) is a chronic inflammatory disorder that presents with both cutaneous manifestations and extracutaneous comorbidities. Current treatment options include antibiotics and biologics; however, treatment failure is common and often surgical intervention is required for acceptable control. Anti-TL1A therapies have recently gained attention in HS treatment due to their ability to inhibit the TL1A/DR3 axis, a key signaling pathway driving immune cell activity and fibrosis. Participant recruitment for the phase 2b trial (NCT06956235) assessing the efficacy of anti-TL1A therapy tulisokibart in moderate-to severe HS was reported on 1 December, 2025 to be completed. This review aims to explore the potential links between the TL1A and HS by synthesizing immune mechanisms of HS pathogenesis with existing data of the TL1A/DR3 axis in immune pathways. A discussion highlighting the potential for anti-TL1A therapies as a class that simultaneously addresses fibrosis and comorbidities of HS is also presented, and future directions to address knowledge gaps are also proposed. - Source: PubMed
Publication date: 2026/04/22
Sia JulingLee BernettOon Hazel H - 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