maintenance and activation mechanisms of memory B cells

2015 Fiscal Year Final Research Report

• Project/Area Number: 24590575
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Immunology
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: ADACHI Takahiro 東京医科歯科大学, 難治疾患研究所, 准教授 (50222625)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: B細胞 / カルシウムシグナル / シグナル伝達 / 生体イメージング

Outline of Final Research Achievements

Ca2+ signaling is one of the typical phenomenon mediated through immune receptors. Analyses of their signaling together with dynamics in vivo is required for understanding of the precise immune responses.I established stable transgenic mice with the genetically encoded Ca2+ indicator yellow cameleon 3.60 (YC3.60) based on the Cre/loxP system. We successfully generated the specific YC3.60 expression mice in immune cells or nerve cells, as well as the ubiquitous expression mice. After crossing with CD19-Cre mice, most B cells exhibited robust YC3.60 expression without significantly altering B-cell function. Intravital imaging of spleen, Peyer’s patches, and bone marrow of the CD19-Cre/YC3.60 mice revealed Ca2+ flux in B cells. B cells exhibiting high Ca2+ were drastically increased in autoimmune-prone CD22 deficient mice. Furthermore, in another autoimmune-prone model C57BL/6-lpr/lpr mouse, lymphocytes of high Ca2+ concentration were increased.

Free Research Field

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