2016 Fiscal Year Final Research Report
Regulation of Mucosal Immunity by CD169 Macrophages
| Project/Area Number |
26460401
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
ASANO Kenichi 東京薬科大学, 生命科学部, 准教授 (10513400)
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| Research Collaborator |
KIKUCHI Kenta 東京薬科大学, 生命科学部
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | マクロファージ / CD169 / 炎症性腸疾患 / CCL8 / 抗体医薬 |
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| Outline of Final Research Achievements |
There are at least 2 subsets of colon macrophages that differ in the expression level of CD169. Selective depletion of CD169 macrophages suppresses DSS-induced colitis in mice. In this study, we revealed that CD169 macrophages produce CCL8 in response to mucosal injury, and that CCL8 recruits inflammatory monocytes to the intestine that furhter aggravate colitis. Administration of anti-CCL8 ameliorates DSS-induced colitis, demonstrating its potential as a novel drug for the treatment of human inflammatory bowel diseases.
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| Free Research Field |
免疫学
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