| Project/Area Number |
15K20333
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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 |
Emergency medicine
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| Research Institution | Chiba University |
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Principal Investigator |
OAMI Takehiko 千葉大学, 大学院医学研究院, 特任助教 (70527887)
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| Research Collaborator |
WATANABE Eizo 千葉大学, 大学院医学研究院, 准教授 (40375639)
ODA Shigeto 千葉大学, 大学院医学研究院, 教授 (90204205)
HATANO Masahiko 千葉大学, 大学院医学研究院, 教授 (20208523)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | オートファジー / アポトーシス / 細胞死 / 敗血症 / 免疫麻痺 / 盲腸結紮穿孔 / 集中治療 |
|---|
| Outline of Final Research Achievements |
In order to elucidate the details of the interaction between autophagy and immunosuppression, we analyzed apoptosis in T cells and survival rate after performing cecal ligation and puncture (CLP) operation on T cell-specific autophagy deficient mice. A blockade of autophagy accelerated T cell apoptosis compared with the control mice, augmenting the gene expression of BIM and PDCD1. Consequently, deficiency of autophagy in T cells significantly decreased the survival rate in the murine sepsis model. In conclusion, we demonstrated that T cell autophagy played a protective role against apoptosis and immunosuppression in sepsis.
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