Maintenace mechanisms of long-lived plasma cells in influenza infectious disease
| Project/Area Number |
25860377
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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 | National Institute of Infectious Diseases |
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Principal Investigator |
Onodera Taishi 国立感染症研究所, その他部局等, 主任研究官 (90513143)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | インフルエンザ感染 / 免疫記憶 / 長期生存型抗体産生細胞 / インフルエンザ / 感染症 / インフルエンザウイルス / ワクチン / インフルエンザウイルス感染症 / B細胞 / 抗体産生細胞 |
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| Outline of Final Research Achievements |
After influenza infection, LLPCs continuously produce virus-specific antibodies with higher affinity for long period of time. They have been maintained constant in their cell number for years in bone marrow (BM), regardless of their limited lifespan (t1/2 ≒ 100 days). We found that LLPCs in BM are replenished by adoptive transferred CD273+ but not CD273- memory B cells, both of which were generated by influenza infection. Moreover, flow cytometric and QPCR analysis demonstrated that the CD273+ memory B cells have the unique expression pattern of chemokine receptors including CCR6 and transcription factors;ZBTB20, ZBTB32, and Smyd2 which are known to be involved in differentiation and maintenance of LLPCs. Thus, these data suggest that the CD273+ memory B cells have the capability to replenish the LLPC pool, probably due to thier unique chemotactic and transcriptional properties, and thereby stabilize the number of LLPCs in BM for long period of time.
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Report
(4 results)
Research Products
(9 results)
