Abstract
Killer cells such as CTL, NK cells, and monocytes play important roles in immune surveillance against transformed cells and virus-infected cells. CTL and NK cells directly kill target cells via two major effector pathways, the perforin-mediated and FasL-mediated pathways. In addition to these pathways, however, some studies by using the gene-targeting mice suggested the possible existence of some other effector mechanisms for the cytotoxicity. Monocytes not only mediate inflammatory responses via production of various cytokines and chemical mediators, but also kill directly some transformed cells. However the effector mechanisms remain largely unknown. Recently, some death-inducing TNF family members, such as TNF-related apoptosis-inducing ligand (TRAIL) and TWEAK were identified and it has been reported that TRAIL- and TWEAK-dependent mechanisms constitute novel pathways of killer cell cytotoxicity. FasL and TRAIL have also been implicated in the tissue damage associated with some inflammatory diseases, such as hepatitis and rheumatoid arthritis. This review describes the expression of FasL, TRAIL, and TWEAK on killer cells and discusses the pathophysiological roles of these molecules in immune system.
