Newly discovered role for Fas ligand in the cell-cycle arrest of CD4(+) T cells

Fas Ligand (FasL) can induce apoptosis of Fas-bearing cells. It is expresse d on the cell surface of many tumor cells, immune-privileged tissues and ac tivated lymphocytes. We report here that Fast can itself transduce signals, leading to cell-cycle arrest and cell death in CD4(+) T cells. In vitro, F ast engagement inhibited CD4(+) T-cell proliferation, cell-cycle progressio n, and IL-2 secretion. In vivo, FasL engagement prevented superantigen-medi ated CD4(+), but not CD8(+), T-cell expansion. These findings demonstrate t hat FasL engagement regulates cell-cycle progression, and show that FasL en gagement in vivo has a potent anti-inflammatory effect specific for CD4(+) T cells.