| Project/Area Number |
15K15288
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Gastroenterology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
NAGAISHI TAKASHI 東京医科歯科大学, 医学部附属病院, 助教 (60447464)
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| Co-Investigator(Kenkyū-buntansha) |
渡辺 守 (渡邉 守) 東京医科歯科大学, 大学院医歯学総合研究科, 教授 (10175127)
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| Research Collaborator |
YAMAZAKI Motomi
ONIZAWA Michio
SUZUKI Masahiro
WATABE Taro
HOSOYA Akinori
TSUGAWA Naoya
JOSE Nisha
KOJIMA Yudai
TOKAI Arisa
TSUGE Naoto
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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 | 炎症性腸疾患 / 粘膜免疫 / オートファジー |
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| Outline of Final Research Achievements |
IBD is characterized by unrestrained lymphocyte activation that results in the production of a variety of pro-inflammatory cytokines and other mediators.Understanding the mechanisms of lymphocyte regulation is therefore of significant importance to dysregulated mucosal inflammation such as IBD.On the other hand, genome-wide association studies in the analysis of IBD have identified genetic risk foci.Especially, several studies have revealed the important roles of autophagy-related genes in IBD, including the suppression of inflammasome in hematopoietic cells and secretion of antimicrobial peptides in Paneth cells.In this regards, we have observed that a lack of autophagy function led to the up-regulated pro-inflammatory cytokines in vivo.Defining the mechanisms of autophagy-mediated T cell regulation will lead to a significant understanding of the manner in which manipulation of this function may provide insights into novel therapeutic methods for the treatment of IBD.
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