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2019 Fiscal Year Final Research Report

Molecular mechanism and regulation in patients with Sjogren's syndrome

Research Project

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Project/Area Number 17K09966
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Collagenous pathology/Allergology
Research InstitutionUniversity of Tsukuba

Principal Investigator

Sumida Takayuki  筑波大学, 医学医療系, 教授 (00183054)

Project Period (FY) 2017-04-01 – 2020-03-31
Keywordsシェーグレン症候群 / Th1細胞 / Treg細胞 / iPS細胞 / ムスカリン作動性アセチルコリン受容体3 / T細胞抗原受容体 / T細胞機能転換分子
Outline of Final Research Achievements

M3R reactive Th1 cells play a crucial role in the generation of Sjogren’s syndrome(SS). In the present study, our object is to clarify the molecules which are able to change Th1 cells to Treg cells. We already generated several T-iPS cells from M3R reactive Th1 cells in patients with SS, induced DC cells from their T-iPS cells, and differentiated CD34+CD43+ progenitor stem cells form T-iPS cells in vitro. In future, we will differentiate CD34+CD43+ cells to Treg cells, and then elucidate the functional molecules which could change from Th1 cells to Treg cells. The candidate molecules should shed light on the new therapeutic approach to SS.

Free Research Field

膠原病学

Academic Significance and Societal Importance of the Research Achievements

シェーグレン症候群(SS)は、ドライアイやドライマウスだけではなく全身の臓器病変を生じる自己免疫疾患である。全身の臓器病変に対する治療は、ステロイドや免疫抑制薬が主体であり、副作用として感染症、悪性腫瘍、生活習慣病、骨粗鬆症などを合併し、QOLの低下が起きてしまうことが問題となっている。本研究の意義は、SSの発症機序に基づいた治療戦略を開発するため、副作用のない疾患特異的な治療薬が創薬され患者さんのQOLの向上が期待されることである。

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Published: 2021-02-19  

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