2005 Fiscal Year Final Research Report Summary
Roles of BCR signaling mediated by PLC-γ2 on memory response
| Project/Area Number |
16590414
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | RIKEN |
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Principal Investigator |
HIKIDA Masaki RIKEN, Laboratory for Lymphocyte Differentiation, Senior Researcher, 分化制御研究グループ, 上級研究員 (60228715)
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| Project Period (FY) |
2004 – 2005
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| Keywords | PLC-γ2 / IgG1 / memory response / class switch / antigen receptor / signal transduction / signaling / conditional knock-out |
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| Research Abstract |
We have crossed the PLC-γ2 conditional knock-out mice with IgG1-Cre expressing mice In order to clarify the roles of PLC-γ2 on memory response. In the B cells from IgG1-Cre mice, only the cells those express γ1 germline transcript express Cre recombinase. For this reason, B cells differentiate normally to mature stage and only those which responded to antigen and switched to IgG1+ express cre recombinase to abolish PLC-γ2 expression. This will make it possible to analyze the role of PLC-γ2 in the IgG1 memory response in comparison with response of other IgG class.
We first examined whether PLC-γ2 gene is efficiently deleted in IgG1 switched cells in vitro or not, and found that it is the case in the mice we have established. Another finding is that IgG1 titer in those mice is markedly decreased in these mice. Together with these results, it is strongly suggested that PLC-γ2 is playing a pivotal role in memory responses.
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