LIGHT/TNFSF14 Protein, Human (HEK293, hFC-Myc)

LIGHT/TNFSF14 protein (CD258; TNFRSF14) is a type II transmembrane protein produced by activated T cells. It is a TNFRSF14/HVEM ligand and belongs to the tumor necrosis factor (TNF) family. LIGHT/TNFSF14 is mainly expressed in spleen, with two subtypes: membrane-bound type and soluble type ^[1]. LIGHT/TNFSF14 protein can be used as immune checkpoint molecule of tumor, and stimulate natural killer cells to produce interferon TFNγ, triggering tumor apoptosis signal ^[2]. LIGHT/TNFSF14 is also involved in the dominant LTβR-NIK-p52 NF-κB pathway promoting the expression of inflammatory gene^[3]. In addition, LIGHT/TNFSF14 protein is a co-stimulatory factor that activates lymphoid cells and has an inhibitory effect on herpes virus infection^[4]. Human LIGHT/TNFSF14 Protein has 240 amino acids and a transmembrane domain (38-58 a.a.). LIGHT/TNFSF14 Protein, Human (HEK293, hFC-Myc) is the extracellular part (D74-V240) of human LIGHT/TNFSF14 Protein, produced by HEK293 cells, with N-terminal hFc- and Myc-tag.

LIGHT/TNFSF14 is a type II transmembrane protein produced by activated T cells, belongs to tumor necrosis factor (TNF) family. LIGHT/TNFSF14 is a TNFRSF14/HVEM (herpesvirus entry mediator) ligand, engages the receptor for the LTalphabeta heterotrimer but does not form complexes with either secreted lymphotoxin alpha (LTalpha) or LTbeta^[1].
LIGHT/TNFSF14 is predominantly expressed in the spleen but also found in the brain. It is 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 tumor lines^[1].
LIGHT/TNFSF14 has a transmemberane, thus it can be leaved into 2 chains: membrane form and soluble form. The soluble form of isoform 1 derives from the membrane form by proteolytic processing.
In tumor immunology, TNFSF14/LIGHT also serves as a novel immune checkpoint molecule for glioblastoma multiforme (GBM), as well as lung carcinoma, breast carcinoma, cervical cancer, and prostate cancer. TNFSF14/LIGHT can stimulate NK cells to produce IFNγ via nuclear factor-κB (NFκB) RelA/p50 signaling. TNFSF14/LIGHT sustains the function of CD8⁺ effector T cells, trigger apoptosis of various tumor cells^[2].
In cell signaling, TNFSF14/LIGHT binds to lymphotoxin-β receptor (LTβR) and HVEM for activating both of them, and disrupts the HVEM-BTLA complex in surface-bound form, and facilitates HVEM-BTLA complex formation in the soluble form^[2].
TNFSF14/LIGHT promotes an inflammatory esophageal fibroblast in vitro via a LTβR-NIK-p52 NF-κB dominant pathway with promoting inflammatory gene expression and down-regulating homeostatic factors including WNTs, BMPs and type 3 semaphorins^[3].
Beside that, TNFSF14/LIGHT protein is a costimulatory factor for the activation of lymphoid cells and as a deterrent to infection by herpesvirus. TNFSF14/LIGHT also prevents tumor necrosis factor alpha mediated apoptosis in primary hepatocyte^[4][5].

Exogenous LIGHT/TNFSF14 (human; 100 ng/mL; 24 h, 48 h, and 96 h) effectively reverses the inhibitory effects of miR-326 overexpression on the expression levels of collagen I and fibronectin, and promotes cell proliferation of TGF-β1-treated airway smooth muscle cells (ASMCs)^[6].
LIGHT/TNFSF14 (human; 100 ng/mL; 24 h) induces increased expression of CD40, CD86, and HLA-DR in stimulation of iDCs (generated in vitro from CD14+ monocytes)^[7].

Measured by its binding ability in a functional ELISA. Immobilized TNFRSF14 at 0.5 μg/mL can bind TNFSF14 at 0.1525-20000 ng/mL, the EC₅₀ is 3.488-13.38 ng/mL.

Human

HEK293

N-hFc;N-Myc

O43557 (D74-V240)

8740  [NCBI]

DGPAGSWEQLIQERRSHEVNPAAHLTGANSSLTGSGGPLLWETQLGLAFLRGLSYHDGALVVTKAGYYYIYSKVQLGGVGCPLGLASTITHGLYKRTPRYPEELELLVSQQSPCGRATSSSRVWWDSSFLGGVVHLEAGEKVVVRVLDERLVRLRDGTRSYFGAFMV

Approximately 46.7 kDa

Greater than 90% as determined by reducing SDS-PAGE.

Lyophilized powder.

Lyophilized from a 0.2 μm sterile filtered PBS, 6% Trehalose, pH 7.4.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O.

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US;may vary elsewhere.

• [1]. Mauri DN, et al. LIGHT, a new member of the TNF superfamily, and lymphotoxin alpha are ligands for herpesvirus entry mediator. Immunity. 1998 Jan;8(1):21-30.  [Content Brief]

  [2]. Han M, et al. Comprehensive characterization of TNFSF14/LIGHT with implications in prognosis and immunotherapy of human gliomas. Front Immunol. 2022 Oct 20;13:1025286.  [Content Brief]

  [3]. Manresa MC, et al. LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms. Mucosal Immunol. 2022 Feb;15(2):327-337.  [Content Brief]

  [4]. Hou Y, et al. Dual Roles of Tumor Necrosis Factor Superfamily 14 in Antiviral Immunity. Viral Immunol. 2022 Nov;35(9):579-585.  [Content Brief]

  [5]. Miao X, et al. HES5-mediated repression of LIGHT transcription may contribute to apoptosis in hepatocytes. Cell Death Discov. 2021 Oct 23;7(1):308.  [Content Brief]

  [6]. Zhang H, et al. TNFSF14, a novel target of miR-326, facilitates airway remodeling in airway smooth muscle cells via inducing extracellular matrix protein deposition and proliferation. Kaohsiung J Med Sci. 2020 Jul;36(7):508-514.  [Content Brief]

  [7]. Holmes TD, et al. Licensed human natural killer cells aid dendritic cell maturation via TNFSF14/LIGHT. Proc Natl Acad Sci U S A. 2014 Dec 30;111(52):E5688-96.  [Content Brief]