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The Journal of Immunology, 1999, 162: 2639-2647.
Copyright © 1999 by The American Association of Immunologists

Involvement of TNF-Related Apoptosis-Inducing Ligand in Human CD4+ T Cell-Mediated Cytotoxicity1

Nobuhiko Kayagaki*, Noriko Yamaguchi*,{dagger}, Masafumi Nakayama*, Akemi Kawasaki*, Hisaya Akiba*,{dagger}, Ko Okumura*,{dagger} and Hideo Yagita2,*,{dagger}

* Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan; and {dagger} Core Research for Evolutional Science and Technology (CREST) of Japan Science and Technology Corp., Tokyo, Japan

TNF-related apoptosis-inducing ligand (TRAIL) has been identified as a member of the TNF family that induces apoptosis in a variety of tumor cells, but its physiological functions are largely unknown. In the present study, we examined the expression and function of TRAIL in human CD4+ T cell clones by utilizing newly established anti-human TRAIL mAbs. Human CD4+ T cell clones, HK12 and 4HM1, exhibited perforin-independent and Fas ligand (FasL)-independent cytotoxicity against certain target cells, including T lymphoma (Jurkat) and keratinocyte (HaCaT) cell lines, which are susceptible to TRAIL-mediated cytotoxicity. In contrast to FasL, the expression of which was inducible upon anti-CD3 stimulation, TRAIL was constitutively expressed on HK12 and 4HM1 cells, and no further increase was observed after anti-CD3 stimulation. Spontaneous cytotoxic activities of resting HK12 and 4HM1 cells against Jurkat and HaCaT cells were blocked by anti-TRAIL mAb but not by anti-FasL mAb, and bystander cytotoxic activities of anti-CD3-stimulated HK12 and 4HM1 cells were abolished by the combination of anti-TRAIL and anti-FasL mAbs. These results indicate a differential regulation of TRAIL and FasL expression on human CD4+ T cell clones and that TRAIL constitutes an additional pathway of T cell-mediated cytotoxicity.




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F. Muhlenbeck, P. Schneider, J.-L. Bodmer, R. Schwenzer, A. Hauser, G. Schubert, P. Scheurich, D. Moosmayer, J. Tschopp, and H. Wajant
The Tumor Necrosis Factor-related Apoptosis-inducing Ligand Receptors TRAIL-R1 and TRAIL-R2 Have Distinct Cross-linking Requirements for Initiation of Apoptosis and Are Non-redundant in JNK Activation
J. Biol. Chem., October 6, 2000; 275(41): 32208 - 32213.
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C. A. Benedict, P. S. Norris, T. I. Prigozy, J.-L. Bodmer, J. A. Mahr, C. T. Garnett, F. Martinon, J. Tschopp, L. R. Gooding, and C. F. Ware
Three Adenovirus E3 Proteins Cooperate to Evade Apoptosis by Tumor Necrosis Factor-related Apoptosis-inducing Ligand Receptor-1 and -2
J. Biol. Chem., January 26, 2001; 276(5): 3270 - 3278.
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