| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Outline of Final Research Achievements |
In order to identify the candidate molecules for the development of the effector cell-targeted treatment for the inhibition of type 1 diabetes, we have developed IL-17/IFN-gamma receptor-double-deficient, Granzyme B-deficient, IRF4-deficient NOD mice. IL-17/IFN-gamma R double-deficiency significantly suppressed the development of diabetes, while independent deletion of IL-17 or IFN-gammaR did not alter the disease susceptibility in NOD mice. Granzyme B-deficient NOD mice spontaneously developed diabetes with similar kinetics to wild-type NOD mice. Diabetes/insulitis and autoantibody production were completely suppressed in IRF4-deficient heterozygous as well as homozygous NOD mice. These suggest that the an IRF4-targeted strategy may be useful for modulating autoimmunity in type 1 diabetes.
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