2018 Fiscal Year Final Research Report
Analyse of Leptin signal in Inflammatory bowel disease
| Project/Area Number |
17K19668
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General internal medicine and related fields
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| Research Institution | Keio University |
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Principal Investigator |
Sujino Tomohisa 慶應義塾大学, 医学部(信濃町), 特任講師 (40464862)
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| Project Period (FY) |
2017-06-30 – 2019-03-31
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| Keywords | 炎症性腸疾患 |
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| Outline of Final Research Achievements |
Leptin is a type of hormone and is known to act on brain, muscle and brown fat cells in the brain after eating, and play a role in insulin sensitivity and suppression of blood sugar elevation. In recent years, it has been discovered that leptin receptors are also present on T cells, and it has been shown that leptin deficiency is less likely to be induced in various enteritis models. The downstream signal of leptin signal is STAT3 pathway, mTOR / Akt pathway, and the former paper has been shown to be essential for Th17 cell induction. We found that the mTOR / AKt signal downstream of leptin is important in the induction of anti-inflammatory CD4CD8aa T cells in the intestinal epithelium.
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| Free Research Field |
消化器内科
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| Academic Significance and Societal Importance of the Research Achievements |
レプチンのレセプター下流のSTAT/mTORについて検討した。CD4特異的にSTAT3を上昇させるSOCSfl/fl:CD4creマウスではCD4CD8aaは有意に減少しない。レプチンシグナル下流におけるmTORに着目して腸管上皮内CD4CD8aa細胞の分化誘導との関連性を検討する。mTORシグナルは細胞内代謝とくに解糖系に必要な分子であり、mTORが活性化することでTh17細胞に分化することが知られている。近年細胞の分化増殖に代謝機構が重要視されており、細胞内の代謝調節という切り口から腸管上皮内の細胞の分化誘導機能を解明することで炎症性腸疾患の病態解明、治療方法を確立できる可能性がある、
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