TNFSF14 Antibody

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Description

Research Applications of TNFSF14 Antibodies

TNFSF14 antibodies are widely used in:

  • ELISA and Western blotting: Detect recombinant or endogenous TNFSF14 with sensitivity down to 0.24 ng/mL .

  • Neutralization assays: Block TNFSF14-induced proliferation of HUVEC cells (ND₅₀: 5–20 ng/mL) .

  • Immunohistochemistry: Study TNFSF14 expression in tumor microenvironments .

Key findings from recent studies:

  • Cancer immunotherapy: TNFSF14-HVEM interactions drive anti-tumor adaptive immunity by normalizing tumor vasculature and enhancing IFN-γ-mediated apoptosis .

  • Antiviral immunity:

    • Reduces mortality in SARS-CoV-2 by neutralizing cytokine storms .

    • Enhances CD8+ T-cell memory against influenza virus .

    • Acts as a proinflammatory factor in hepatitis infections .

  • NK cell-DC crosstalk: Licensed NK cells (expressing self-MHC-reactive receptors) produce TNFSF14 to mature dendritic cells, linking innate and adaptive immunity .

Table 1: Neutralization of TNFSF14-Induced HUVEC Proliferation

Antibody (Catalog #)TNFSF14 Concentration (ng/mL)Proliferation Inhibition (%)
AF664 (Detection)1095%
AF664 + MAB664210<5% (ND₅₀: 5–20 ng/mL)
Data adapted from R&D Systems .

Table 2: Western Blot Sensitivity of Anti-TNFSF14 Antibody (ab233502)

TNFSF14 Protein (ng)Band Intensity (Relative Units)
250100%
15.62545%
0.24Detectable threshold
Data sourced from Abcam .

Therapeutic Implications

  • Cancer: TNFSF14 antibodies are investigated for:

    • Normalizing tumor vasculature .

    • Sensitizing tumors to checkpoint inhibitors .

  • Viral infections: Anti-TNFSF14 monoclonal antibodies reduce COVID-19 mortality by 40% in preclinical models .

Key Challenges and Future Directions

  • Dual roles in immunity: TNFSF14 exhibits pro-inflammatory effects in hepatitis but protective roles in influenza .

  • Clinical translation: Optimal dosing and receptor targeting (HVEM vs. LTβR) require further validation .

Product Specs

Buffer
The antibody is provided as a liquid solution in phosphate-buffered saline (PBS) containing 50% glycerol, 0.5% bovine serum albumin (BSA), and 0.02% sodium azide.
Form
Liquid
Lead Time
Typically, we are able to dispatch orders within 1-3 business days after receiving them. However, delivery times may vary depending on the specific purchasing method or location. For detailed information on delivery times, please contact your local distributors.
Synonyms
TNFSF14; HVEML; LIGHT; UNQ391/PRO726; Tumor necrosis factor ligand superfamily member 14; Herpes virus entry mediator ligand; HVEM-L; Herpesvirus entry mediator ligand; CD antigen CD258
Target Names
Uniprot No.

Target Background

Function
TNFSF14 (TNF Superfamily Member 14), also known as LIGHT (Lymphotoxin-like, inducible expression, and competes with glycoprotein D for herpesvirus entry mediator), is a cytokine that binds to TNFRSF3/LTBR (Lymphotoxin-beta Receptor). This binding can modulate the effects of TNFRSF6B, a decoy receptor. LIGHT also acts as a ligand for TNFRSF14/HVEM (Herpesvirus Entry Mediator). Upon binding to HVEM, LIGHT delivers costimulatory signals to T cells, promoting T cell proliferation and the production of interferon-gamma (IFNG).
Gene References Into Functions
  • This study provides compelling evidence that TNFSF14 is crucial for limiting key steps in the pathogenesis of metabolic syndrome. These findings support the development of TNFSF14 signaling agonists as promising therapeutics for treating obesity and type 2 diabetes. PMID: 29359470
  • LIGHT is highly expressed in patients with coronary disease, often accompanied by severe inflammation. LIGHT significantly enhances the inflammatory response in oxLDL-induced THP-1 macrophages. PMID: 28642135
  • The interaction between LIGHT and LTBR promotes the survival and proliferation of human bone marrow-derived mesenchymal stem cells. This suggests that LIGHT may play a significant role in stem cell therapy. PMID: 27835685
  • Serum LIGHT levels correlate with the progression and severity of interstitial pneumonia in patients with dermatomyositis. PMID: 26448572
  • Through LTbetaR signaling, LIGHT may contribute to the exacerbation of airway neutrophilic inflammation by stimulating cytokine and chemokine production in bronchial epithelial cells. PMID: 25501580
  • LIGHT regulates the production of thymic stromal lymphopoietin (TSLP) to drive pulmonary fibrosis. PMID: 25680454
  • The tumor necrosis factor superfamily molecule LIGHT promotes keratinocyte activity and skin fibrosis. PMID: 25789702
  • Overexpression of TNFSF14 in Tca8113 cells enhances cell proliferation and migration. PMID: 26146063
  • LIGHT, a member of the TNF superfamily, is involved in T-cell homeostasis and erosive bone disease associated with rheumatoid arthritis. PMID: 25460501
  • Crystal structures of LIGHT and the LIGHT:DcR3 complex reveal the structural basis for DcR3-mediated neutralization of LIGHT. PMID: 25087510
  • Regulation by NK cell licensing helps to prevent TNFSF14 production in response to healthy tissues. PMID: 25512551
  • These findings suggest a novel molecular determinant of LIGHT-mediated pathogenic changes in human bronchial epithelial cells. PMID: 25251281
  • TNFSF14 interacts with bronchial epithelial cells, influencing the activation of basophils and eosinophils. PMID: 24782592
  • Triggering of LIGHT induces the production of pro-inflammatory mediators, such as interleukin-8 and matrix metalloproteinase-9, while suppressing phagocytic activity. PMID: 24044961
  • Individuals carrying the GG genotype of rs1077667 in the LIGHT gene, associated with the highest risk for Multiple Sclerosis, exhibit the lowest serum LIGHT levels. PMID: 23037546
  • While a limited number of activated T-cells infiltrate tumors and initiate an immune response, the number of LIGHT+ T cells infiltrating the tumor is very low. PMID: 23514280
  • These findings demonstrate that LIGHT is not inhibited by osteoprotegerin (OPG), a soluble RANKL receptor. LIGHT is a potent osteoclastogenesis factor that activates the Akt, NFkappaB, and JNK pathways. PMID: 23391709
  • TNFSF14 is significantly elevated in sickle-cell anemia (SCA) patients, including those treated with hydroxycarbamide and HbSC. This increase may contribute to endothelial activation and inflammation in SCA. PMID: 22775554
  • This study revealed that expression of the death-triggering ligand LIGHT is increased in the spinal cords of patients with Amyotrophic Lateral Sclerosis (ALS). PMID: 22221541
  • Increased plasma LIGHT levels have been observed in patients with atopic dermatitis. PMID: 22519595
  • INF-gamma can synergistically precede LIGHT-induced apoptotic processes through down-regulation of Bcl-2 expression, but not survivin expression. This process may be caspase (especially caspase-3)-independent, although extensive caspase activation is observed. PMID: 21117871
  • These data clearly indicate that ZFP91 is a key regulator in LIGHT-induced activation of the non-canonical NF-kappaB pathway in LTbetaR signaling. PMID: 20804734
  • Herpes simplex virus 1 gD interferes with HVEM function by competing with its natural ligands and downregulating HVEM. PMID: 20826693
  • Increased potential for LIGHT receptor signaling, coupled with increased bioavailability due to lower decoy receptor-3 (DcR3) avidity, provides a mechanism for polymorphic variants in LIGHT to contribute to the pathogenesis of inflammatory diseases. PMID: 20592286
  • LIGHT mediates organ-specific donor T cells activation in Graft-versus-Host Disease (GVHD). PMID: 19826934
  • LIGHT suppresses tumor growth by augmenting immune response. PMID: 19716382
  • There is overexpression of genes related to immune and inflammatory responses, including cytokines such as TNFSF14, in interstitial cystitis. PMID: 20096889
  • When highly expressed, LIGHT is capable of promoting effector T cell proliferation and differentiation even in a regulatory T (Treg) cell-enriched, suppressive intestinal environment. PMID: 20042587
  • These findings suggest that LIGHT may be involved in the progression of inflammatory bone destruction in rheumatoid arthritis. PMID: 19019090
  • Effects in transgenic mice indicate that human LIGHT may function as a major regulator of T cell activation, implicating LIGHT signaling pathways in inflammation focused on mucosal tissues. PMID: 11714797
  • LIGHT (TNFSF14), and its membrane-anchored ligand, were also present in atheromatous lesions, with the highest concentrations found in regions rich in macrophage-derived foam cells. PMID: 11742858
  • The role of the calcium-signaling pathway in the transcriptional control of LIGHT is investigated. PMID: 12215452
  • LIGHT may act as an anti-apoptotic agent against TNFalpha-mediated liver injury by blocking the activation of both caspase-3 and caspase-8. PMID: 12393901
  • A review of LIGHT, a new member of the TNF superfamily. PMID: 12456019
  • Data show that mRNA encoding LIGHT and its receptors (HVEM, LTbetaR, and TR6 (DcR3)) are present in placentas and cytotrophoblast cells at term. PMID: 12466117
  • Soluble LIGHT blocks TR6-Fc costimulated proliferation, lymphokine production, and cytotoxicity of T cells in the presence of T cell receptor ligation. PMID: 12471113
  • LIGHT-sensitized IFN-gamma-mediated apoptosis of MDA-MB-231 cells is probably through down-regulation of anti-apoptosis Bcl-2 family members. It could be caspase (especially caspase-3)-independent, even though extensive caspase activation was observed. PMID: 12767529
  • LIGHT signaling is mediated through both death receptor and mitochondria pathways. PMID: 15115612
  • LIGHT-herpesvirus entry mediator mediated signaling as an important immune regulatory mechanism in mucosal inflammatory responses. PMID: 15210782
  • Mechanisms protecting trophoblast cells from LIGHT-mediated apoptosis were studied. PMID: 15215185
  • LIGHT expression by human intestinal T cells suggests the possibility that LIGHT may play a key role in the regulation of the mucosal immune system. PMID: 15634882
  • LIGHT protein can be activated on mucosal T cells through a gut-specific CD2-dependent signaling mechanism. PMID: 15634882
  • Data suggest that LIGHT constitutively expressed in human melanoma cells and microvesicles may contribute to the regulation of T-cell responses to tumor cells. PMID: 15833878
  • NF-kappaB signaling plays a key role in LIGHT-mediated upregulation of CD86 expression. PMID: 15895390
  • Both LTbetaR and HVEM can discriminatively mediate the expression of different genes in cultured human umbilical vein endothelial cells, including LIGHT, a proinflammatory cytokine. PMID: 15917993
  • A transgenic mouse model resembling Crohn's disease (CD) suggests that up-regulation of LIGHT may be a critical mediator of CD pathogenesis. PMID: 15944326
  • LIGHT could serve as a molecular link between lipid metabolism, inflammation, and thrombus formation, all of which are features of atherosclerotic plaques. PMID: 16186421
  • Platelet-derived LIGHT is biologically active and can induce an inflammatory response in monocytes and particularly within endothelial cells, as measured by the up-regulation of adhesion molecules and the release of chemokines. PMID: 16861346
  • Blockade of TNFSF14 signaling caused a substantial reduction in the expression of lymphotoxin beta receptor (LTbetaR)-controlled migration factors within the islets and disrupts organization of tertiary structures, leading to the prevention of diabetes. PMID: 16934497
  • The LIGHT system may regulate early to middle stages of placental development through cell-specific, temporally programmed expression of the ligand and its receptors. This system may also contribute to maintaining placental immune privilege. PMID: 17010447
Database Links

HGNC: 11930

OMIM: 604520

KEGG: hsa:8740

STRING: 9606.ENSP00000469049

UniGene: Hs.129708

Protein Families
Tumor necrosis factor family
Subcellular Location
[Tumor necrosis factor ligand superfamily member 14, membrane form]: Cell membrane; Single-pass type II membrane protein.; [Tumor necrosis factor ligand superfamily member 14, soluble form]: Secreted.; [Isoform 2]: Cytoplasm.
Tissue Specificity
Predominantly expressed in the spleen but also found in the brain. Weakly expressed in peripheral lymphoid tissues and in heart, placenta, liver, lung, appendix, and kidney, and no expression seen in fetal tissues, endocrine glands, or nonhematopoietic tu

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