Fas ligand: a potential target for therapeutic immune modulation in transplantation and inflammatory diseases

Abstract

Fas ligand (FasL) triggers apoptosis of cells expressing its cognate receptor, Fas (CD95/APO-1). FasL precludes inflammatory reactions from immune privileged sites by inducing Fas-mediated apoptosis of infiltrating pro-inflammatory cells. The ability of FasL to impair immune responses is showing therapeutic promise as a possible means of protecting tissue transplants from immunological rejection. However, FasL is becoming an enigmatic molecule, exhibiting pro-inflammatory activity independently of its ability to mediate immune privilege. FasL can recruit and activate neutrophils in some situations. FasL appears to contribute to destruction of Fas-sensitive end-organ cells during inflammation. Prevention of Fas-mediated end-organ apoptosis and enhancement of Fas-mediated apoptosis of inflammatory cells are emerging as potential anti-inflammatory therapeutic goals.

• antisense
• apoptosis
• arthritis
• caspase inhibitors
• Fas (CD95/APO-1)
• Fas ligand (FasL)
• immune privilege
• inflammation
• inflammatory bowel disease
• neutrophil
• soluble FasL (sFasL)
• transplantation