Intracellular trafficking mechanisms regulating the level of antigen presentation in dendritic cells
Project/Area Number |
17K08273
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Biological pharmacy
|
Research Institution | Okayama University |
Principal Investigator |
Furuta Kazuyuki 岡山大学, 医歯薬学総合研究科, 准教授 (50644936)
|
Project Period (FY) |
2017-04-01 – 2021-03-31
|
Project Status |
Completed (Fiscal Year 2020)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | 樹状細胞 / MHC-II / エンドサイトーシス / Rab11 / 小胞輸送 / 抗原提示 / Rab / 免疫学 / 細胞生物学 |
Outline of Final Research Achievements |
Dendritic cells induce an immune response by presenting pathogen-derived antigens to T cells by major histocompatibility antigen class II (MHC-II). The cell surface expression level of MHC-II is a regulator of the immune response. We have previously found that crosslinking of MHC-II by the TCR of activated T cells induces endocytosis of MHC-II. In this study, we analyzed the signaling mechanism induced by MHC-II crosslinking. We found that crosslinking of MHC-II induces calcium influx via activation of Syk/PLC, resulting in clathrin-dependent endocytosis of MHC-II mediated with PKC activation.
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Academic Significance and Societal Importance of the Research Achievements |
本研究によって、MHC-IIの細胞表面からのダウンレギュレーション機構として、カルシウム流入によるPKCの活性化を介した、クラスリン依存的エンドサイトーシスという新たなMHC-IIのエンドサイトーシスを誘導する機構が明らかとなった。今後、MHC-IIの発現異常の関連する疾患において、MHC-IIの発現調節の標的となる可能性が考えられる。
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Report
(5 results)
Research Products
(18 results)