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CXCL10 DNA Vaccination Prevents Spontaneous Diabetes through Enhanced Cell Proliferation in NOD Mice¹

Toshikatsu Shigihara^*, Akira Shimada^2,*, Yoichi Oikawa^*, Hiroyuki Yoneyama, Yasuhiko Kanazawa^*, Yoshiaki Okubo^*, Kouji Matsushima, Eiji Yamato, Jun-ichi Miyazaki, Akira Kasuga, Takao Saruta^* and Shosaku Narumi

^* Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan; Department of Molecular Preventive Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan; Division of Stem Cell Regulation Research, Area of Molecular Therapeutics, Course of Advanced Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan; and Department of Internal Medicine, Tokyo Denryoku Hospital, Tokyo, Japan

CXCL10, a chemokine for Th1 cells, is involved in the pathogenesis of various Th1-dominant autoimmune diseases. Type 1 diabetes is considered to be a Th1-dominant autoimmune disease, and a suppressive effect of CXCL10 neutralization on diabetes development has been reported in a cyclophosphamide-induced accelerated diabetes model through induction of cell proliferation. However, intervention in a diabetes model might bring about opposite effects, depending on the timing, amount, or method of treatment. In the present study, we examined the effect of CXCL10 neutralization in a "spontaneous diabetes" model of NOD mice, using CXCL10 DNA vaccination (pCAGGS-CXCL10). pCAGGS-CXCL10 treatment in young NOD mice induced the production of anti-CXCL10 Ab in vivo and suppressed the incidence of spontaneous diabetes, although this treatment did not inhibit insulitis or alter the immunological response. pCAGGS-CXCL10 treatment enhanced the proliferation of pancreatic cells, resulting in an increase of cell mass in this spontaneous diabetes model as well. Therefore, CXCL10 neutralization is suggested to be useful for maintaining cell mass at any stage of autoimmune diabetes.

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