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Blood, 1 October 2004, Vol. 104, No. 7, pp. 2051-2059.
Prepublished online as a Blood First Edition Paper on April 27, 2004; DOI 10.1182/blood-2003-10-3485.
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Submitted October 14, 2003
Accepted March 31, 2004
Natural Killer T Cells Accelerate Atherogenesis in Mice
Yukihito Nakai, Kazuya Iwabuchi*, Satoshi Fujii, Naoki Ishimori, Nyambayar Dashtsoodol, Keiko Watano, Tetsuya Mishima, Chikako Iwabuchi, Shinya Tanaka, Jelena S Bezbradica, Toshinori Nakayama, Masaru Taniguchi, Sachiko Miyake, Takashi Yamamura, Akira Kitabatake, Sebastian Joyce, Luc Van Kaer, and Kazunori Onoe
Division of Immunobiology, Research Section of Pathophysiology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Hokkaido, Japan; Department of Cardiovascular Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan
Division of Immunobiology, Research Section of Pathophysiology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Hokkaido, Japan
Department of Cardiovascular Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan
Division of Immunobiology, Research Section of Pathophysiology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Hokkaido, Japan; Department of Cardiovascular Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan; The Jackson Laboratory, Bar Harbor, ME, USA
Laboratory of Molecular and Cellular Pathology, Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan
Department of Microbiology and Immunology, School of Medicine, Vanderbilt University, Nashville, TN, USA
Department of Immunology, Graduate School of Medicine, Chiba University, Chiba, Chiba, Japan
Laboratory of Immune Regulation, RIKEN Research Center for Allergy and Immunology, Yokohama, Kanagawa, Japan
Department of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Kodaira, Tokyo, Japan
* Corresponding author; email: akimari{at} imm.hokudai.ac.jp.
We have investigated the potential role of CD1d-restricted natural killer T (NKT) cells in the development of atherosclerosis in mice. When fed an atherogenic diet (AD), NKT cell-deficient CD1d-/- mice had significantly smaller atherosclerotic lesions than AD-fed C57BL/6 (WT) mice. A significant reduction of atherosclerotic lesions was also demonstrated in AD-fed, low-density lipoprotein receptor deficient (Ldlr-/-) mice reconstituted with CD1d-/- bone marrow cells, as compared with the lesions observed in Ldlr-/- mice reconstituted with WT marrow cells. In addition, repeated injection of  -GalCer or the related glycolipid OCH to apolipoprotein E knockout (apoE-/-) mice during the early phase of atherosclerosis significantly enlarged the lesion areas compared to mice injected with vehicle control. However, administration of -GalCer to apoE-/- mice with established lesions did not significantly increase the lesion area, but considerably decreased the collagen content. Development of atherosclerosis in either AD-fed WT or apoE-/- mice was associated with the presence of V14J18 transcripts in the atherosclerotic arterial walls, indicating that NKT cells were recruited to these lesions. Thioglycolate-elicited macrophages pulsed with oxidized low-density lipoproteins expressed enhanced CD1d levels and induced NKT cells to produce interferon- , a potentially pro-atherogenic Th1 cytokine. Collectively, we conclude that NKT cells are pro-atherogenic in mice.
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