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International Immunology Advance Access originally published online on July 21, 2008
International Immunology 2008 20(9):1231-1237; doi:10.1093/intimm/dxn080
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© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Protection of IFN-{gamma} signaling-deficient NOD mice from diabetes by cyclophosphamide

Yoshiko Mori1, Takako Kato1, Tetsuro Kodaka1, Edith M. Kanagawa1, Shohei Hori2 and Osami Kanagawa1

1 Laboratory for Autoimmune Regulation
2 Research Unit for Immune Homeostasis, RIKEN Center for Allergy and Immunology, RIKEN Yokohama Institute, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan

Correspondence to: O. Kanagawa; E-mail: kanagawa{at}rcai.riken.jp

Non-obese diabetic (NOD) mice that are genetically deficient in either IFN-{gamma} or β chain of the IFN-{gamma}R develop diabetes with similar kinetics to wild-type NOD mice. In the current study, we demonstrated that treatment of IFN-{gamma} signaling-deficient NOD mice with cyclophosphamide (CY) not only fails to induce acute diabetes but also confers permanent protection from diabetes. Protection was mediated by the preferential generation of regulatory T cells (Treg cells) that are capable of suppressing the diabetogenic process, with no change in the total number and function of Treg cells. Moreover, CY treatment of IFN-{gamma} signaling-deficient NOD mice reversed the ongoing pathogenic process and eliminated cellular infiltrates of pancreatic islets. While these results have been derived using a genetically modified mouse model of diabetes, they indicate that knowledge of host genetic factors and environmental factors influencing the development of Type I diabetes mellitus may provide a rational approach to develop a means to reverse the development of Type I diabetes in human.

Keywords: environmental factor, genetic factor, regulatory T cell, Type I diabetes

Transmitting editor: S. Izui

Received 8 February 2008, accepted 20 June 2008.


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