Fas Ligand antibody [101624]

Fas Ligand (Fas ligand, FasL, CD95L), a 40 kDa type II membrane protein, belongs to the tumor necrosis factor (TNF) family, 2 which includes TNF alpha, and the alpha and betachains of lymphotoxin (LT), CD40 ligand, and CD30 ligand. In the new TNF superfamily nomenclature, FasL is referred to as TNFSF6. The specific receptor for FasL is Fas (CD95, Apo-1), a 45 kDa type I membrane protein that is a member of the TNF receptor family. FasL has four potential N-glycosylation sites which appear to be variably used. 3 Consequently, the apparent molecular weight of FasL may vary, per glycosylation and breakdown patterns in a certain preparation. The amino acid sequences of human and murine FasL are 76.9% identical, and they are not species-specific. Membrane bound FasL (mFasL) is a 40 kDa protein, while the active soluble form of FasL (sFasL) was identified as a 26 kDa protein from the supernatant of activated peripheral T cells and cultured cells transfected with the full-length FasL DNA. Like other members of the TNF family membrane-bound FasL can be cleaved to generate the soluble Fas ligand, a non-covalently linked homotrimer. Membrane-bound FasL and TNFalpha are primary activators of their receptors. Soluble FasL may inhibit the killing effect of membrane FasL. The Fas/ FasL system plays an important role in modulating immune response by inducing cell apoptosis to maintain homeostasis, self-tolerance of lymphocytes, and immune privilege. Engagement of Fas by its ligand, results in the rapid induction of programmed cell death (PCD) in susceptible cells. This process bypasses the usual long sequence of signaling enzymes and immediately activates preexisting caspases. Fas Ligand is a potent chemoattractant for neutrophils, suggesting that it has a proinflammatory function. FasL is predominantly expressed on activated T cells and NK cells, whereas Fas is expressed on various cell types. The activation of mature T cells with phorbol myristic acetate (PMA) and ionomycin, concanavalin A (Con A) or anti-CD3, induces FasL gene expression. Herpes Simplex virus type 2 (HSV-2) but not HSV-1, potentially inhibits FasL surface expresssion in infected cells and thereby suppresses FasL-mediated cell death.