LIGHT is a member of the TNF family which includes TNF-α, TNF-β (lymphotoxin-alpha, LT-α), CD40 ligand, TRAIL (Apo2L), Fas ligand (FASL), and osteoprotegerin (OPG) ligand. LIGHT is a type II transmembrane protein that possesses 34% identity with lymphotoxin beta (LT-β), and shares a 31% identity with FASL. LIGHT stimulates the proliferation of activated HVEM+ T-cells, NF-κB activation, and induces apoptosis in cells expressing both HVEM+ and LT-β receptors. B- and T- lymphocyte attenuators (BTLA) also bind to HVEM. LIGHT, as well as other members of the TNF/TNFR family, is released from the membrane by MMPs. It plays a key role for optimal IL-12 production by the dendritic cells (DCs) and the development of IFN-γ-producing CD4+ Th1 cells. Bone marrow-derived DCs from LIGHT (-/-) mice are severely impaired in IL-12p40 production after IFN-γ and LPS stimulation in vitro. LIGHT is expressed in lung inflammatory leukocytes after an allergen house dust mite challenge. It induces airway remodeling via the induction of TGF-β. The inhibition of LIGHT, using a fusion protein of Fc with the extracellular portion of the LT-β receptor (LTβ R-Fc), prevents LIGHT-LTβ R and LIGHT-HVEM interaction. In a mouse model of chronic asthma, this reduces lung fibrosis, smooth muscle and epithelial hyperplasia, and airway hyper-responsiveness through the suppression of lung TGF-β and IL-13 production. LIGHT has been shown to increase the anti-tumor immune response and its overexpression is associated with the survival in patients with colorectal cancer liver metastasis.