| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Outline of Final Research Achievements |
Systemic sclerosis (SSc) is characterized by three pathological features, including immune abnormalities/inflammation, vasculopathy, and fibrosis. A series of our studies demonstrated that Fli1 deficiency contributes to the development of vasculopathy and fibrosis of SSc, but the role of Fli1 deficiency in immune abnormalities/inflammation still remains unknown. Therefore, to address this issue, we here investigated the impact of Fli1 deficiency on myeloid cells. Our results demonstrated the following findings: (i) Fli1 deficiency promotes the differentiation of macrophages into M2 subtype, (ii) myeloid cell-specific Fli1 knockout (Fli1 MyeKO) mice spontaneously develop dermal fibrosis due to endothelial-to-mesenchyaml transition following initial vascular changes, (iii) Fli1 MyeKO mice exhibit Th2/Th17-skewed immune polarization. Taken together, these results indicate that myeloid Fli1 deficiency is involved in the development of the three cardinal pathological features of SSc.
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