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2014 Fiscal Year Final Research Report

Investigation on the role of nicotinic acetylcholine receptors in regulation of inflammatory and immune responses

Research Project

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Project/Area Number 24590120
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Biological pharmacy
Research InstitutionKitasato University

Principal Investigator

KAWASHIMA Koichiro  北里大学, 薬学部, 客員教授 (70095008)

Co-Investigator(Kenkyū-buntansha) FUJII Takeshi  同志社女子大学, 薬学部, 教授 (80255380)
HORIGUCHI Kazuhide  福井大学, 医学部, 准教授 (20377451)
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)
Project Period (FY) 2012-04-01 – 2015-03-31
Keywordsアセチルコリン / ニコチン受容体 / T細胞 / 樹状細胞 / Th0 / SLURP-1 / Th1 / alpha7
Outline of Final Research Achievements

In the current project, we investigated the localization of SLURP-1, an endogenous allosteric ligand for alpha7 nAChRs, in immune organs and its role in regulation of T cell function together with effects of nicotine on T cell differentiation. Using immunohistochemical techniques, we found specific SLURP-1 localization in CD205-positive dendritic cells residing in the marginal zone of the human tonsil. SLURP-1 attenuated the growth of human leukemic T cell line MOLT-3 cells and human blood mononuclear cells (MNLs), but increased ACh synthesis in these cells, suggesting facilitation of functional development of T cells by SLURP-1. Nicotine suppressed differentiation of Th0 cells to Tregs, but facilitated to Th1 in mouse spleen MNLs, suggesting a role for nAChRs in T cell differentiation.
These results suggest that SLURP-1 plays a role in T cell development and differentiation during antigen presentation through stimulation of alpha7 nAChRs.

Free Research Field

薬理学

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Published: 2016-06-03  

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