A potential role of autophagy in immune cells during sepsis

Research Project

Project/Area Number	15K20333
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Emergency medicine
Research Institution	Chiba University
Principal Investigator	OAMI Takehiko 千葉大学, 大学院医学研究院, 特任助教 (70527887)
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)
Project Period (FY)	2015-04-01 – 2017-03-31
Project Status	Completed (Fiscal Year 2016)
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)
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.