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-α and IFN-β), and neither type II IFN (IFN-γ) 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.
Skip Nav Destination
Article navigation
3 May 1999
Article|
May 03 1999
Type I Interferons (IFNs) Regulate Tumor Necrosis Factor–related Apoptosis-inducing Ligand (TRAIL) Expression on Human T Cells: A Novel Mechanism for the Antitumor Effects of Type I IFNs
Nobuhiko Kayagaki,
Nobuhiko Kayagaki
From the *Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan; ‡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
Search for other works by this author on:
Noriko Yamaguchi,
Noriko Yamaguchi
From the *Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan; ‡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
Search for other works by this author on:
Masafumi Nakayama,
Masafumi Nakayama
From the *Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan; ‡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
Search for other works by this author on:
Hiroshi Eto,
Hiroshi Eto
From the *Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan; ‡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
Search for other works by this author on:
Ko Okumura,
Ko Okumura
From the *Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan; ‡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
Search for other works by this author on:
Hideo Yagita
Hideo Yagita
From the *Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan; ‡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
Search for other works by this author on:
Nobuhiko Kayagaki
From the *Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan; ‡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
Noriko Yamaguchi
From the *Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan; ‡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
Masafumi Nakayama
From the *Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan; ‡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
Hiroshi Eto
From the *Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan; ‡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
Ko Okumura
From the *Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan; ‡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
Hideo Yagita
From the *Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan; ‡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
Address correspondence to Hideo Yagita, Department of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan. Phone: 81-3-3818-9284; Fax: 81-3-3813-0421; E-mail: [email protected]
Received:
February 02 1999
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1999
J Exp Med (1999) 189 (9): 1451–1460.
Article history
Received:
February 02 1999
Citation
Nobuhiko Kayagaki, Noriko Yamaguchi, Masafumi Nakayama, Hiroshi Eto, Ko Okumura, Hideo Yagita; Type I Interferons (IFNs) Regulate Tumor Necrosis Factor–related Apoptosis-inducing Ligand (TRAIL) Expression on Human T Cells: A Novel Mechanism for the Antitumor Effects of Type I IFNs . J Exp Med 3 May 1999; 189 (9): 1451–1460. doi: https://doi.org/10.1084/jem.189.9.1451
Download citation file:
Sign in
Don't already have an account? Register
Client Account
You could not be signed in. Please check your email address / username and password and try again.
Could not validate captcha. Please try again.
Sign in via your Institution
Sign in via your InstitutionSuggested Content
Email alerts
Advertisement