The Journal of Experimental Medicine
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Published online 26 September 2005. doi:10.1084/jem.20050448
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© The Rockefeller University Press, 0022-1007
The Journal of Experimental Medicine

Brief Definitive Report

V{alpha}14 NK T cell–triggered IFN-{gamma} production by Gr-1+CD11b+ cells mediates early graft loss of syngeneic transplanted islets

Yohichi Yasunami1, Satoshi Kojo3, Hiroshi Kitamura4, Atsushi Toyofuku1,5, Masayuki Satoh1, Masahiko Nakano1, Kentaroh Nabeyama1, Yoshiichiroh Nakamura1, Nobuhide Matsuoka1, Seiyo Ikeda1, Masao Tanaka5, Junko Ono2, Naoki Nagata6, Osamu Ohara4, and Masaru Taniguchi3

1 Department of Surgery I, Fukuoka University School of Medicine, Jonan-ku, Fukuoka 814-0180, Japan
2 Laboratory Medicine, Fukuoka University School of Medicine, Jonan-ku, Fukuoka 814-0180, Japan
3 Laboratory for Immune Regulation, RIKEN Research Center for Allergy and Immunology, Tsurumi-ku, Yokohama 230-0045, Japan
4 Laboratory for Immunogenomics, RIKEN Research Center for Allergy and Immunology, Tsurumi-ku, Yokohama 230-0045, Japan
5 Department of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8582, Japan
6 Department of Surgery I, School of Medicine, University of Occupational and Environmental Health, Yahatanisi-ku, Kitakyushu 807-8555, Japan

CORRESPONDENCE Masaru Taniguchi: taniguti{at}rcai.riken.jp

Pancreatic islet transplantation is a highly promising approach for the treatment of insulin-dependent diabetes mellitus. However, the procedure remains experimental for several reasons, including its low efficiency caused by the early graft loss of transplanted islets. We demonstrate that Gr-1+CD11b+ cells generated by transplantation and their IFN-{gamma} production triggered by V{alpha}14 NKT cells are an essential component and a major cause of early graft loss of pancreatic islet transplants. Gr-1+CD11b+ cells from V{alpha}14 NKT cell–deficient (J{alpha}281–/–) mice failed to produce IFN-{gamma}, resulting in efficient islet graft acceptance. Early graft loss was successfully prevented through the repeated administration of {alpha}-galactosylceramide, a specific ligand for V{alpha}14 NKT cells, resulting in dramatically reduced IFN-{gamma} production by Gr-1+CD11b+ cells, as well as V{alpha}14 NKT cells. Our study elucidates, for the first time, the crucial role of Gr-1+CD11b+ cells and the IFN-{gamma} they produce in islet graft rejection and suggests a novel approach to improving transplantation efficiency through the modulation of V{alpha}14 NKT cell function.


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