2017 Fiscal Year Final Research Report
Role of SLURP-1, an endogenous alpha7 nicotinic acetylcholine receptor allosteric ligand, in T cell differentiation
| Project/Area Number |
15K07969
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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 |
Pharmacology in pharmacy
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
藤井 健志 同志社女子大学, 薬学部, 教授 (80255380)
間下 雅士 同志社女子大学, 薬学部, 助教 (30738886)
堀口 和秀 福井大学, 学術研究院医学系部門, 准教授 (20377451)
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| Co-Investigator(Renkei-kenkyūsha) |
MISAWA Hidemi 慶応大学, 薬学部, 教授 (80219617)
MORIWAKI Yasuhiro 慶応大学, 薬学部, 講師 (00392150)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | ｎACｈR / アロステリック・リガンド / Treg / Th1 / Th2 / GTS-21 / alpha7 / DO11.10マウス |
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| Outline of Final Research Achievements |
We studied roles of GTS-21, an alpha7 (a7) nAChR agonist, and recombinant human type SLURP-1 (rhSLURP-1), an endogenous allosteric a7 nAChR ligand, in regulation of T cell differentiation. The differentiation was activated by culturing spleen cells from DO11.10 mice with ovalbumin (OVA) or OVA peptide (OVA-P). The effects of GTS-21 and rhSLURP-1 on T cell differentiation into regulatory T cell (Tregs) and effector T cells (Th1 and Th2) were determined by FACS or ELISA. GTS-21 inhibited the differentiation into Tregs and effector T cells under OVA activation, but facilitated the differentiation under OVA-P activation. rhSLURP-1 did not show any effect under the present experimental conditions. These results suggest that a7 nAChR activation in antigen-presenting cells prevents antigen processing leading to suppression of the differentiation while a7 nAChR activation in T cell facilitates the differentiation. No effect with rhSLURP-1 may be due to species difference.
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| Free Research Field |
薬理学
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