| Project/Area Number |
15K19138
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Immunology
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| Research Institution | Tokyo University of Science |
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Principal Investigator |
Haniuda Kei 東京理科大学, 研究推進機構生命医科学研究所, 助教 (40734918)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 免疫学 / アレルギー / IgE / 胚中心 / メモリーB細胞 / 長期生存プラズマ細胞 / 免疫記憶 / B細胞受容体 / プラズマ細胞 |
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| Outline of Final Research Achievements |
It is well known that dysregulated production of IgE can be a cause of allergic disorders. Normally, the differentiation of IgE+ B cells into memory-B or long-lived plasma cells is suppressed by unknown mechanisms. However, it has been unclear how the propensity of IgE+ B cells toward short-lived fate is induced. In this study, I revealed molecular mechanisms how the autonomous signaling of membrane IgE (mIgE) suppresses B-cell maintenance. I found that CH1-4 domain of mIgE spontaneously induces cell death through the activation of Syk-BLNK axis and membrane proximal domain of mIgE promotes plasma cell differentiation through CD19-pathway. I also demonstrated that defects of the mIgE-signaling could be a cause of allergy.
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