Gut homeostasis regulated by epithelia-immune cell interaction
Project/Area Number |
18K07184
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 49070:Immunology-related
|
Research Institution | Toho University |
Principal Investigator |
Naito Taku 東邦大学, 医学部, 准教授 (10568728)
|
Project Period (FY) |
2018-04-01 – 2022-03-31
|
Project Status |
Completed (Fiscal Year 2021)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
Keywords | T細胞 / エピジェネティクス / 腸上皮間リンパ球 / IEL / ホーミング / T細胞分化 / 細胞接着 / Eed / インテグリン / 腸管上皮 / 腸管恒常性 |
Outline of Final Research Achievements |
The role of Eed, a mediator of repressive histone modification, in differentiation and maintenance of intraepithelial lymphocytes (IELs) was examined. Loss of Eed in mouse resulted in the trend of increased CD4+ CD8+ IEL. In vitro culture system identified a cell adhesion molecule as an enhancing factor of CD4+ CD8+ IEL differentiation, which was further enhanced by Eed heterozygous deletion. In addition, loss of Eed affected differentiation/survival of CD4+ but not much of CD8+ IELs. These results suggested that the interaction between cell adhesion molecule and epigenetic machinery plays a role in the gut homeostasis.
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Academic Significance and Societal Importance of the Research Achievements |
腸管は無害・有害を問わず恒常的に異物にさらされており、その恒常性の維持は個体の生存にとって重要である。腸管恒常性維持を担う分子機構の解明は、炎症性腸疾患(IBD)の新規治療作用点の同定につながることが期待される。本研究では従来からIBDの治療標的となってきた細胞接着分子がエピジェネティックな分子機構を介して腸管恒常性維持を制御していることを示唆しており、IBDの新たな治療標的候補としての抑制的ヒストン修飾の可能性を示した。
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Report
(5 results)
Research Products
(9 results)