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J. Exp. Med.,
Volume 189, Number 9, May 3, 1999 1451-1460
By



From the * Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo
113-8421, Japan; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a proapoptotic
member of the TNF family of type II membrane proteins, which constitutes one component of
T cell cytotoxicity. In this study, we investigated the expression and function of TRAIL in human peripheral blood T (PBT) cells. Although freshly isolated PBT cells did not express a detectable level of TRAIL on their surface, a remarkable TRAIL expression was rapidly induced on the surface of both CD4+ and CD8+ PBT cells upon stimulation with anti-CD3 monoclonal antibody and type I interferons (IFNs). This enhancement of TRAIL expression was a
unique feature of type I IFNs (IFN-
Core Research for Evolutional Science and Technology (CREST), Japan Science
and Technology Corporation (JST), Chiyoda-ku, Tokyo 101-0062, Japan; and the § Department of
Urology, Kobe University School of Medicine, Chuo-ku, Hyogo 650-0017, Japan
and IFN-
), and neither type II IFN (IFN-
) nor various other cytokines enhanced TRAIL expression on anti-CD3-stimulated PBT cells. Type I
IFNs have been used for clinical treatment of renal cell carcinomas (RCCs), and we found that
most RCC cell lines were susceptible to TRAIL-induced apoptosis. Type I IFNs substantially
augmented cytotoxic activity of anti-CD3-stimulated PBT cells against RCC cell lines in a
TRAIL-dependent manner. These results indicate a unique feature of type I IFNs to regulate
TRAIL-mediated T cell cytotoxicity, which may be involved in the antitumor effects of type I
IFNs against various tumors.
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