| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
Systemic sclerosis (SSc), or scleroderma, is a chronic connective tissue disease characterized by three cardinal features: autoimmunity/inflammation, vasculopathy, and fibrosis in the skin and various internal organs. Although SSc pathogenesis remains elusive, genetic studies have demonstrated the central role of immune abnormalities in SSc development. In particular, recent researches have disclosed the cardinal role of innate immune system dysregulation in the pathogenesis of autoimmune diseases including SSc.
Numerous studies from our laboratory and others have demonstrated the critical role of Friend leukemia virus integration 1 (Fli1), a member of the Ets transcription factor family, in SSc pathogenesis. This time, we studied on the correlation between Fli1 and dysregulation in the innate immune system in SSc, and indeed could demonstrate their profound relationship in its pathogenesis.
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