2023 Fiscal Year Final Research Report
Immune cell-like functions of epithelial cells induced by MHC-I signal
| Project/Area Number |
21H02768
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 50010:Tumor biology-related
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| Research Institution | Tokyo University of Pharmacy and Life Science (2023)
Waseda University (2021-2022) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
大庭 賢二 自治医科大学, 医学部, 講師 (20759576)
河野 恵子 沖縄科学技術大学院大学, 膜生物学ユニット, 准教授 (30632723)
藤枝 俊宣 東京工業大学, 生命理工学院, 准教授 (70538735)
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| Project Period (FY) |
2021-04-01 – 2024-03-31
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| Keywords | 貪食様取込 / 発がん制御 |
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| Outline of Final Research Achievements |
We have found that epithelial cells not only recognize the MHC-I of cells with membrane damage (MDed cells) and eliminate them through extrusion but also through phagocytosis-like engulfment. Therefore, the aim is to i) elucidate the mechanism by which MDed cells are engulfed by neighboring normal cells. Furthermore, we aim to expand to ii) identify what other extracellular stresses, besides membrane damage, are involved. By constructing a novel peptide array screening system, we have identified candidate molecules as key cell-cell interaction molecules in the mechanism. Based on this, we have identified the core ligands and receptors that trigger phagocytosis-like engulfment, shedding light on a part of the mechanism.
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| Free Research Field |
腫瘍生物学
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| Academic Significance and Societal Importance of the Research Achievements |
がん変異細胞の排除、さらには発がんに関わる異常細胞を排除するメカニズムの解明は、「がんを予防する」という観点から必須であり、新規診断法の確立へと繋がると期待できる。これまで見出したalpha3ペプチドや、本研究課題の成果から創出されるであろう貪食様取込みの促進薬などが、まさにこのがん変異細胞を強力に排除する可能性があり、今後予防的にがん変異細胞や異常細胞を排除する医療の確立の道をひらくと期待される。
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