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Tumor necrosis factor (ligand) superfamily, member 14
Available structures
PDB Ortholog search: PDBe, RCSB
Symbols TNFSF14 ; CD258; HVEML; LIGHT; LTg; TR2
External IDs OMIM604520 MGI1355317 HomoloGene2822 GeneCards: TNFSF14 Gene
RNA expression pattern
PBB GE TNFSF14 207907 at tn.png
More reference expression data
Species Human Mouse
Entrez 8740 50930
Ensembl ENSG00000125735 ENSMUSG00000005824
UniProt O43557 Q9QYH9
RefSeq (mRNA) NM_003807 NM_019418
RefSeq (protein) NP_003798 NP_062291
Location (UCSC) Chr 19:
6.66 – 6.67 Mb
Chr 17:
57.19 – 57.19 Mb
PubMed search [1] [2]

Tumor necrosis factor ligand superfamily member 14 is a protein that in humans is encoded by the TNFSF14 gene.[1][2] TNFSF14 has also been designated as CD258,[citation needed] as well as LIGHT.[3]

The protein encoded by this gene is a member of the tumor necrosis factor (TNF) ligand family. This protein is a ligand for TNFRSF14, which is a member of the tumor necrosis factor receptor superfamily, and which is also known as a herpesvirus entry mediator ligand (HVEML). This protein may function as a costimulatory factor for the activation of lymphoid cells and as a deterrent to infection by herpesvirus. This protein has been shown to stimulate the proliferation of T cells, and trigger apoptosis of various tumor cells. This protein is also reported to prevent tumor necrosis factor alpha mediated apoptosis in primary hepatocyte. Two alternatively spliced transcript variant encoding distinct isoforms have been reported.[2]


TNFSF14 has been shown to interact with TNFRSF14,[4][5] TNFRSF6B,[4][5][6] BIRC2,[7] TRAF2[7] and TRAF3.[7]

Role in herpes simplex virus[edit]

Similar to how CD4 is the primary mediating receptor in HIV infection, the HSV glycoprotein (gD) binds to the HVEM receptor which is demanded by TNFSF14/LIGHT lowering the ability for LIGHT to activate the NFκB pathway. NFκB is a survival factor helping to inhibit apoptosis which triggers a pathway inhibiting caspase 8. When gD from HSV binds to HVEM, LIGHT is non-competitively inhibited from binding, encouraging apoptosis in the infected cell.[3]


  1. ^ Mauri DN, Ebner R, Montgomery RI, Kochel KD, Cheung TC, Yu GL, Ruben S, Murphy M, Eisenberg RJ, Cohen GH, Spear PG, Ware CF (February 1998). "LIGHT, a new member of the TNF superfamily, and lymphotoxin alpha are ligands for herpesvirus entry mediator". Immunity 8 (1): 21–30. doi:10.1016/S1074-7613(00)80455-0. PMID 9462508. 
  2. ^ a b "Entrez Gene: TNFSF14 tumor necrosis factor (ligand) superfamily, member 14". 
  3. ^ a b Ware, Carl (2008). "Chapter 25: TNF-Related Cytokines in Immunity". In Paul, William. Fundamental Immunology (Book) (6th ed.). Philadelphia: Lippincott Williams & Wilkins. pp. 776–801. ISBN 0-7817-6519-6. 
  4. ^ a b Zhang, J; Salcedo T W, Wan X, Ullrich S, Hu B, Gregorio T, Feng P, Qi S, Chen H, Cho Y H, Li Y, Moore P A, Wu J (June 2001). "Modulation of T-cell responses to alloantigens by TR6/DcR3". J. Clin. Invest. (United States) 107 (11): 1459–68. doi:10.1172/JCI12159. ISSN 0021-9738. PMC 209323. PMID 11390428. 
  5. ^ a b Yu, K Y; Kwon B; Ni J; Zhai Y; Ebner R; Kwon B S (May 1999). "A newly identified member of tumor necrosis factor receptor superfamily (TR6) suppresses LIGHT-mediated apoptosis". J. Biol. Chem. (UNITED STATES) 274 (20): 13733–6. doi:10.1074/jbc.274.20.13733. ISSN 0021-9258. PMID 10318773. 
  6. ^ Hsu, Tsui-Ling; Chang Yung-Chi; Chen Siu-Ju; Liu Yong-Jun; Chiu Allen W; Chio Chung-Ching; Chen Lieping; Hsieh Shie-Liang (May 2002). "Modulation of dendritic cell differentiation and maturation by decoy receptor 3". J. Immunol. (United States) 168 (10): 4846–53. doi:10.4049/jimmunol.168.10.4846. ISSN 0022-1767. PMID 11994433. 
  7. ^ a b c Kuai, Jun; Nickbarg Elliott; Wooters Joe; Qiu Yongchang; Wang Jack; Lin Lih-Ling (April 2003). "Endogenous association of TRAF2, TRAF3, cIAP1, and Smac with lymphotoxin beta receptor reveals a novel mechanism of apoptosis". J. Biol. Chem. (United States) 278 (16): 14363–9. doi:10.1074/jbc.M208672200. ISSN 0021-9258. PMID 12571250. 

Further reading[edit]

External links[edit]

This article incorporates text from the United States National Library of Medicine, which is in the public domain.