Elucidation of mechanisms for B-cell fate decision by membrane IgE signaling

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19138
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Immunology
• Research Institution: Tokyo University of Science
• 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)
• Project Period (FY): 2015-04-01 – 2017-03-31
• 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

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.

Free Research Field

免疫学