Expression and Function of TNF-Related Apoptosis-Inducing Ligand on Murine Activated NK Cells

TNF-related apoptosis-inducing ligand (TRAIL), a new member of TNF family, induces apoptotic cell death of various tumor cells. We recently showed that TRAIL mediates perforin- and Fas ligand (FasL)-independent cytotoxic activity of human CD4+ T cell clones. In the present study, we investigated the...

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Bibliographic Details
Published in:The Journal of immunology (1950) 1999-08, Vol.163 (4), p.1906-1913
Main Authors: Kayagaki, Nobuhiko, Yamaguchi, Noriko, Nakayama, Masafumi, Takeda, Kazuyoshi, Akiba, Hisaya, Tsutsui, Hiroko, Okamura, Haruki, Nakanishi, Kenji, Okumura, Ko, Yagita, Hideo
Format: Article
Language:English
Subjects:
Animals
Antibodies, Monoclonal - chemistry
Antibodies, Monoclonal - metabolism
Apoptosis - genetics
Apoptosis - immunology
Apoptosis Regulatory Proteins
Cell Line
Cytotoxicity, Immunologic
Humans
Interleukin-15 - pharmacology
Interleukin-2 - pharmacology
Killer Cells, Natural - immunology
Killer Cells, Natural - metabolism
Ligands
Lymphocyte Activation - genetics
Male
Membrane Glycoproteins - biosynthesis
Membrane Glycoproteins - genetics
Membrane Glycoproteins - immunology
Membrane Glycoproteins - metabolism
Mice
Mice, Inbred C57BL
Rats
Rats, Inbred F344
Recombinant Proteins - biosynthesis
Recombinant Proteins - chemistry
Recombinant Proteins - immunology
Recombinant Proteins - metabolism
TNF-Related Apoptosis-Inducing Ligand
Transfection
Tumor Cells, Cultured
Tumor Necrosis Factor-alpha - biosynthesis
Tumor Necrosis Factor-alpha - genetics
Tumor Necrosis Factor-alpha - immunology
Tumor Necrosis Factor-alpha - metabolism
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Summary:TNF-related apoptosis-inducing ligand (TRAIL), a new member of TNF family, induces apoptotic cell death of various tumor cells. We recently showed that TRAIL mediates perforin- and Fas ligand (FasL)-independent cytotoxic activity of human CD4+ T cell clones. In the present study, we investigated the expression and function of TRAIL on murine lymphocytes by using newly generated anti-murine TRAIL mAbs. Although freshly isolated T, B, or NK cells did not express a detectable level of TRAIL on their surface, a remarkable level of TRAIL expression was induced preferentially on CD3- NK1.1+ NK cells after stimulation with IL-2 or IL-15. In contrast, TRAIL expression was not induced by IL-18, whereas it efficiently potentiated lymphokine-activated killer activity of NK cells. In addition to perforin inactivation and neutralization of FasL by anti-FasL mAb, neutralization of TRAIL by anti-TRAIL mAb was needed for the complete inhibition of IL-2- or IL-15-activated NK cell cytotoxicity against mouse fibrosarcoma L929 target cells, which were susceptible to both FasL and TRAIL. These results indicated preferential expression of TRAIL on IL-2- or IL-15-activated NK cells and its potential involvement in lymphokine-activated killer activity.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.163.4.1906