Reorganization of differentiation lineage by searching for SatM precursor
Project/Area Number |
17K19557
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Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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Allocation Type | Multi-year Fund |
Research Field |
Pathology, Infection/Immunology, and related fields
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Research Institution | Osaka University |
Principal Investigator |
Satoh Takashi 大阪大学, 免疫学フロンティア研究センター, 准教授 (60619716)
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Project Period (FY) |
2017-06-30 – 2020-03-31
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Project Status |
Completed (Fiscal Year 2019)
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Budget Amount *help |
¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2019: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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Keywords | 線維症 / マクロファージ / 自然免疫 / 分化 / 細胞分化 / 疾患特異的マクロファージ / アレルギー / メタボリックシンドローム / 疾患 / 創薬 / 転写因子 |
Outline of Final Research Achievements |
fibrosis is a life-threatening disease of unknown aetiology. Its pathogenesis is poorly understood and there are no effective therapy. We have previously identified SatM as a new macrophage/monocyte involved in the development of fibrosis. Here we show that SatM differentiates from SMP, a precursor that differs from known macrophage precursors (MDP and cMoP). Furthermore, we found that NF-IL6 deficient SMP was not proliferate, it was revealed that NF-IL6 functions in SMP and that these cells can proliferate. From the above, we have clarified a part of the onset mechanism of fibrosis that has not been clarified so far.
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Academic Significance and Societal Importance of the Research Achievements |
線維症は体の生命維持に必要な肺、肝臓、心臓、腎臓、皮膚などで起こり、その臓器としての機能が著しく損なわれる。また、これまで線維症に有効な治療法は殆ど報告されていない。本研究では、同定した線維化の発症に重要な自然免疫系の新しい細胞であるSegregated nucleus containing atypical monocyte:SatMの分化メカニズムを同定した。またNF-IL6が欠損したマウスではSatMが末梢から無くなり、線維化が抑制されるが、この分子の作用点がSatMの前駆体である事を明らかにした。以上の事から、本研究により未解明であった線維化の発症メカニズムの一端が明らかになった。
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Report
(4 results)
Research Products
(63 results)
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[Journal Article] Identification of an atypical monocyte and committed progenitor involved in fibrosis.2017
Author(s)
Satoh T, Nakagawa K, Sugihara F, Kuwahara R, Ashihara M, Yamane F, Minowa Y, Fukushima K, Ebina I, Yoshioka Y, Kumanogoh A, Akira S
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Journal Title
Nature
Volume: 541
Issue: 7635
Pages: 96-101
DOI
Related Report
Peer Reviewed / Open Access
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