| Project/Area Number |
24591378
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Hematology
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| Research Institution | Nippon Medical School (2014)
Hirosaki University (2012-2013) |
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Principal Investigator |
WADA Ryuichi 日本医科大学, 医学部, 准教授 (20260408)
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| Co-Investigator(Kenkyū-buntansha) |
YAJIMA Nobuhisa 弘前大学, 医学研究科, 研究員 (30443980)
IMAIZUMI Tadaatsu 弘前大学, 医学研究科, 教授 (90232602)
SATO Tsugumi 弘前大学, 医学研究科, 助教 (40733001)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | Hodgkin lymphoma / Epstein Barr virus / RIG-I / IRF3 / Interferon / regulatory T cell / cytotoxic T cell / innate immunity / interferon / CCL20 / BZLF1 / BRLF1 / EBER / Type 1 interferon / Tumor microebvironment |
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| Outline of Final Research Achievements |
Epstein-Barr virus (EBV) infection is associated in about half cases of classical Hodgkin lymphoma (CHL). The aim of the study is explore the molecular alteration of intracellular innate immunity for the development of new therapeutic strategy of CHL. In the tumor microenvironment of EBV-positive CHL, regulatory T cells were increased, while cytotoxic T cells were reduced. The expression of a pattern recognition receptor RIG-I was increased, but activation of IRF3 and expression of interferon were not found in EBV-positive CHL. The interruption of RIG-I signaling may be associated with the immediate early genes derived from EBV. Further, the expression of inhibitory chemokine CCL20 was increased in EBV-positive CHL. The latent infection of EBV alter innate immunity signaling and modulate the tumor microenvironment to immunosuppressive state. It is considered that he amelioration of intracellular innate immunity is a possible therapeutic strategy for CHL.
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