Fas ligand (FasL) is produced by activated T cells and natural killer cells
and it induces apoptosis (programmed cell death) in target cells through t
he death receptor Fas/Apo1/CD95 (ref. 1). One important role of Fast and Fa
s is to mediate immune-cytotoxic killing of cells that are potentially harm
ful to the organism, such as virus-infected or tumour cells(1). Here we rep
ort the discovery of a soluble decoy receptor, termed decoy receptor 3 (DcR
3), that binds to Fast and inhibits Fast-induced apoptosis. The DcR3 gene w
as amplified in about half of 35 primary lung and colon tumours studied, an
d DcR3 messenger RNA was expressed in malignant tissue. Thus, certain tumou
rs may escape FasL-dependent immune-cytotoxic attack by expressing a decoy
receptor that blocks FasL.