| Project/Area Number |
24790384
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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 |
Experimental pathology
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| Research Institution | Osaka University |
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Principal Investigator |
MATSUMOTO Masanori 大阪大学, 免疫学フロンティア研究センター, 特任助教 (50542106)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 免疫 / plasmablasts / IL-10 / 脳脊髄炎 / 多発性硬化症 / 国際研究者交流 |
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| Research Abstract |
B cells can suppress experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, by secreting the anti-inflammatory cytokine IL-10. However, which B cell subsets can serve as IL-10-producing B cells to suppress EAE remains unknown. By using IL-10 reporter mice, we found that plasmablasts in the draining lymph nodes (dLNs) predominantly expressed IL-10 during EAE. In addition, mice lacking plasmablasts developed an exacerbated EAE. Thus, these results suggest that plasmablasts in the dLNs can serve as IL-10 producers to limit EAE inflammation.
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