2024 Fiscal Year Final Research Report
The mechanism of MHC-I specific induction on cancer immunity
| Project/Area Number |
23K19476
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Multi-year Fund |
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| Review Section |
0803:Pathology, infection/immunology, and related fields
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Project Period (FY) |
2023-08-31 – 2025-03-31
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| Keywords | NLRC5 / MHC class I |
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| Outline of Final Research Achievements |
Major histocompatibility complexes (MHC) are crucial molecles to initiate immune response against tumors. Expression of MHC-I, which is required for cytotoxity by CD8 T cells, is regulated by NLRC5. NLRC5 shares DNA banding factors with MHC-II transcrptional factor, CIITA, because NLRC5 have no domain to bind DNA. However, MHC expression regulated by NLRC5 is MHC-I,not MHC-II. In currect study, I investigated using a protein binding NLRC5, and have defined the mechanism how NLRC5 induce sinagistically the expression in MHC-I and its associated genes.
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| Free Research Field |
腫瘍免疫学
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| Academic Significance and Societal Importance of the Research Achievements |
MHCは獲得免疫において不可欠な因子であり、その発現機構の解明は免疫学を研究する上で重要である。転写活性化因子NLRC5はMHC-Iとその関連遺伝子の転写を特異的に活性化するが、そのメカニズムはわかっておらず、その解明が本研究の目的であった。本研究では、新規タンパク質とNLRC5の複合体が、MHC-I発現を選択的に、かつ相乗的に誘導することが明らかになった。これにより、NLRC5に加えて、このタンパク質も癌などで治療標的になり得ることが示唆された。
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