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LIGHT /TNFSF14

LIGHT (derived from “homologous to Lymphotoxins, exhibits Inducible expression, and competes with Herpes simplex virus (HSV) Glycoprotein D for Herpes virus entry mediator (HVEM /TR2), a receptor expressed by T lymphocytes”) is a 29 kDa type 2 transmembrane protein that belongs to the TNF superfamily [1, 2] and is expressed in granulocytes, monocytes, immature dendrtic cells and activated T cells. LIGHT is active either as membrane-anchored or secreted (soluble) forms. Three receptors of the TNF superfamily: lymphotoxin receptor (LTR), herpesvirus entry mediator (HVEM), and decoy receptor 3 (DcR3) binds to the ligand. LIGHT is involved in T-cell regulation and dendritic cell maturation [3]. It triggers several signaling pathways such as NF-kB, non-canonical NF-kB, Stat3, ERK5 / BMK1 and the mitogen-activated protein (MAP) kinase JNK [4]. LIGHT is released from platelets and induces a proinflammatory state in vascular endothelial cells [5]. It suppress tumor formation in vivo by inducing apoptotic cell death. Embryonic stem (ES) cells are differentiated in the presence of LIGHT [6]. Mice overexpressing LIGHT spontaneously develop severe autoimmune disease . LIGHT has been reported to increase in Rhumatoid Arthritis (RA) patient s and induce a RANKL -dependent and -independent osteoclasts formation [7].

LIGHT, Soluble (human) Detection Set (APO-54N-029)

Summary of features

	For the quantitative determination of human soluble (secreted) LIGHT (human) from biological fluids (serum, plasma and cell culture supernatant)
	Detection limit: 0.2 ng/ml
	Range: 0-20 ng/ml
	Specificity : Detects only human LIGHT /TNFSF14
	Format: sufficient materials to run ELISAs on 5 x 96-well plates

Principle of the Kit

This assay is a sandwich Enzyme Linked-Immuno-Sorbent Assay (ELISA) developed for the direct measurement of human LIGHT (hLIGHT) in biological fluids. A monoclonal antibody specific for hLIGHT (COAT) is coated onto the wells of the microtiter plate. Samples and standards of hLIGHT are pipetted into the wells for binding to the coated antibody. After extensive washing to remove unbound compounds, hLIGHT is recognized by the addition of a biotinylated monoclonal antibody specific for hLIGHT (DET). After removal of excess biotinylated antibody, streptavidine-peroxidase is added. Following a final washing, peroxidase activity is quantified using the substrate 3,3’,5,5’-tetramethylbenzidine (TMB). The intensity of the color reaction is measured at 450 nm after acidification and is directly proportional to the concentration of hLIGHT in the samples.

Figure: Linearity of the standard curve

LITERATURE OVERVIEW:

1. Granger, S.W., and Rickert, S. (2003). LIGHT-HVEM signaling and the regulation of T cell-mediated immunity. Cyt. & Growth Fact. R. 14, 289-296.

2. Mauri, D.N., Ebner, R., Montgomery, R.I., Kochel, K.D., Cheung, T.C., Yu, G.L., Ruben, S., Murphy, M., Eisenberg, R.J., Cohen, G.H., et al. (1998). LIGHT, a new member of the TNF superfamily, and lymphotoxin alpha are ligands for herpesvirus entry mediator. Immunity 8, 21-30.

3. Tamada, K., Shimozaki, K., Chapoval, A.I., Zhai, Y., Su, J., Chen, S.F., Hsieh, S.L., Nagata, S., Ni, J., and Chen, L. (2000). LIGHT, a TNF-like molecule, costimulates T cell proliferation and is required for dendritic cell-mediated allogeneic T cell response. J Immunol. 164, 4105-4110.

4. Nadiminty, N., Chun, J.Y., Hu, Y., Dutt, S., Lin, X., and Gao, A.C. (2007). LIGHT, a member of the TNF superfamily, activates Stat3 mediated by NIK pathway. BBRC 359, 379-384.

5. Otterdal, K., Smith, C., Oie, E., Pedersen, T.M., Yndestad, A., Stang, E., Endresen, K., Solum, N.O., Aukrust, P., and Damas, J.K. (2006). Platelet-derived LIGHT induces inflammatory responses in endothelial cells and monocytes. Blood 108, 928-935.

6. Zou, G.M., Chen, J.J., and Ni, J. (2006). LIGHT induces differentiation of mouse embryonic stem cells associated with activation of ERK5. Oncogene 25, 463-469.

7. Edwards, J.R., Sun, S.G., Locklin, R., Shipman, C.M., Adamopoulos, I.E., Athanasou, N.A., and Sabokbar, A. (2006). LIGHT (TNFSF14), a novel mediator of bone resorption, is elevated in rheumatoid arthritis. Arth, and Rheum. 54, 1451-1462.