Selection of B cells by novel signaling molecule selectively expressed in IgG+ B cells
| Project/Area Number |
16K08834
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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 |
Immunology
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| Research Institution | Akita University |
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Principal Investigator |
Hikida Masaki 秋田大学, 理工学研究科, 教授 (60228715)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 記憶Ｂ細胞 / 抗原受容体 / シグナル伝達 / アポトーシス / 胚中心 / 遺伝子発現 / 記憶応答 / Ｂ細胞 / Parm1 / NPxYモチーフ / チロシンリン酸化 / 細胞内輸送 / 免疫応答 / シグナル分子 / 免疫学 / 細胞 / 発現制御 |
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| Outline of Final Research Achievements |
When immune responses were examined by reconstituted mice, whose B cells were derived from Parm1-deficeint mice, secondary responses were markedly diminished, which was in contrast with relatively normal primary response.
In addition, roles of Parm1 in BCR signaling were examined using Parm1-deficient A20 B cell line and it was revealed that BCR signaling followed by Ca2+ influx was significantly augmented in Parm1-deficient cells. Further, weak phosphorylation signal of ITIM motif in Parm1 was induced by BCR stimulation.
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| Academic Significance and Societal Importance of the Research Achievements |
これまで、未熟Ｂ細胞においては強い抗原受容体（ＢＣＲ）架橋によってアポトーシスに陥るのに対して、抗原に対して高親和性を獲得した記憶Ｂ細胞が当該抗原によってＢＣＲを架橋されても死ぬことはなく逆に活性化される分子メカニズムは明らかになっていなかった。本研究の成果により、IgG陽性記憶Ｂ細胞においては、IgM陽性Ｂ細胞では発現していないParm1が発現しており、この分子の働きによりアポトーシスが回避されていることが世界で初めて明らかとなった。
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Report
(4 results)
Research Products
(4 results)
