| Project/Area Number |
25860813
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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 |
Collagenous pathology/Allergology
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 自己抗体 / B-1細胞 / 胚中心 / 自己免疫疾患 |
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| Outline of Final Research Achievements |
Autoimmunity is associated with the generation of high affinity auto-antibodies (Abs) that are strongly reactive to self-antigens and class switching, typically with IgG class Abs produced by long-lived plasma cells. Peritoneal B-1a cells, which often produce the IgM class Abs cross-react with self-Ag, are thought to be the source of auto-Ab-producing long-lived plasma cells because various autoimmune-prone mice show the abnormal expansion of peritoneal B-1a cells. In this study, we demonstrated that B-1a cells could differentiate into IgG auto-Ab producing plasma cells in the germinal center like environment. In addition, abnormal expression of G5PR, which is regulatory molecule for B cell receptor signaling, enhanced the differentiation of B-1a cells into auto-Ab producing cells . Thus, the regulation of cell signaling by G5PR in B-1a cells might be a critical target to prevent auto-Ab production in autoimmune diseases.
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