Fas/Fas ligand on the road: an apoptotic pathway common to AIDS, autoimmunity, lymphoproliferation and transplantation

There is considerable interest in the role of Fas protein as it induces apo ptotic cell death when ligated by its natural ligand (FasL). Interaction between Fas and Fast is a crucial mechanism for clonal deletion and immune tolerance and privilege, control of T cell expansion during imm une responses and killing by cytotoxic T lymphocytes. Loss of function of t he system can block lymphocyte apoptosis and cause lymphoproliferation and autoimmunity but, when the system overfunctions, it can end to tissue injur y and destruction. Recent studies have demonstrated that the Fas/FasL system is implicated in the pathogenesis of several human diseases ranging from AIDS to autoimmunit y and lymphoproliferation, hepatitis, multiple sclerosis and transplant rej ection. It is conceivable that modulating the activity of the Fas/fasL pathway woul d have clinical applications for the treatment of these patients.