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Department of Pathogenic Biochemistry, Research Institute of Natural Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan;
Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan;
Core Research for Evolutional Science and Technology of Japan Science and Technology Corporation, Tokyo, Japan; and
Department of Microbiology and Immunology, Howard Hughes Medical Institute, Vanderbilt University School of Medicine, Nashville, TN 37232
V
14 NKT cells produce large amounts of IFN-
and IL-4 upon
recognition of their specific ligand -galactosylceramide
(-GalCer) by their invariant TCR. We show here that NKT cells
constitutively express CD28, and that blockade of CD28-CD80/CD86
interactions by anti-CD80 and anti-CD86 mAbs inhibits the
-GalCer-induced IFN- and IL-4 production by splenic V14 NKT
cells. On the other, the blockade of CD40-CD154 interactions by
anti-CD154 mAb inhibited -GalCer-induced IFN- production, but
not IL-4 production. Consistent with these findings, CD28-deficient
mice showed impaired IFN- and IL-4 production in response to
-GalCer stimulation in vitro and in vivo, whereas production of
IFN- but not IL-4 was impaired in CD40-deficient mice. Moreover,
-GalCer-induced Th1-type responses, represented by enhanced
cytotoxic activity of splenic or hepatic mononuclear cells and
antimetastatic effect, were impaired in both CD28-deficient mice and
CD40-deficient mice. In contrast, -GalCer-induced Th2-type
responses, represented by serum IgE and IgG1 elevation, were impaired
in the absence of the CD28 costimulatory pathway but not in the absence
of the CD40 costimulatory pathway. These results indicate that
CD28-CD80/CD86 and CD40-CD154 costimulatory pathways differentially
contribute to the regulation of Th1 and Th2 functions of V14 NKT
cells in vivo.
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Y. Hayakawa, K. Takeda, H. Yagita, M. J. Smyth, L. Van Kaer, K. Okumura, and I. Saiki IFN-gamma -mediated inhibition of tumor angiogenesis by natural killer T-cell ligand, alpha -galactosylceramide Blood, August 13, 2002; 100(5): 1728 - 1733. [Abstract] [Full Text] [PDF]
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Z. Trobonjaca, A. Kroger, D. Stober, F. Leithauser, P. Moller, H. Hauser, R. Schirmbeck, and J. Reimann Activating Immunity in the Liver. II. IFN-{beta} Attenuates NK Cell-Dependent Liver Injury Triggered by Liver NKT Cell Activation J. Immunol., April 15, 2002; 168(8): 3763 - 3770. [Abstract] [Full Text] [PDF]
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M. J. Smyth, N. Y. Crowe, D. G. Pellicci, K. Kyparissoudis, J. M. Kelly, K. Takeda, H. Yagita, and D. I. Godfrey Sequential production of interferon-gamma by NK1.1+ T cells and natural killer cells is essential for the antimetastatic effect of alpha -galactosylceramide Blood, February 15, 2002; 99(4): 1259 - 1266. [Abstract] [Full Text] [PDF]
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A. K. Singh, M. T. Wilson, S. Hong, D. Olivares-Villagomez, C. Du, A. K. Stanic, S. Joyce, S. Sriram, Y. Koezuka, and L. Van Kaer Natural Killer T Cell Activation Protects Mice Against Experimental Autoimmune Encephalomyelitis J. Exp. Med., December 17, 2001; 194(12): 1801 - 1811. [Abstract] [Full Text] [PDF]
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K. Kawakami, Y. Kinjo, K. Uezu, S. Yara, K. Miyagi, Y. Koguchi, T. Nakayama, M. Taniguchi, and A. Saito Monocyte Chemoattractant Protein-1-Dependent Increase of V{alpha}14 NKT Cells in Lungs and Their Roles in Th1 Response and Host Defense in Cryptococcal Infection J. Immunol., December 1, 2001; 167(11): 6525 - 6532. [Abstract] [Full Text] [PDF]
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