The mechanism of memory B-cell disturbance in cirrhosis
| Project/Area Number |
25860563
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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 |
Gastroenterology
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| Research Institution | Showa 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 |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 記憶B細胞 / 肝硬変 / 免疫不全 / B細胞レセプター / 液性免疫 / 免疫グロブリン / TLR9 / TLR4 / 免疫異常 / バクテリアルトランスロケーション / フローサイトメトリー |
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| Outline of Final Research Achievements |
Not only CD27+ memory B-cell but also CD4+ and CD8+ effector memory T-cell are reduced in cirrhotic patients compared to healthy donors. These loss of memory B and T-cell are larger as hepatic function becomes exacerbated and could be a cause of immunodeficiency observed in cirrhosis.
Memory B-cell is apt to get activated and be resistant to apoptosis compared to Naive B-cell. B-cell receptor signaling is the most potent factor for, especially Naive, B-cell activation and survival. BCR signal also kept higher CD27 expression on B-cell. The weaker BCR signaling could be a cause of CD27+ memory B-cell loss in cirrhotic patients. Interestingly, though the strongest stimulation in this experimental setting induced great activation marker elevation, it also induced more apoptosis. We believe the optimal balance of stimulation is very important for the best B-cell activation and survival.
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Report
(3 results)
Research Products
(4 results)
