2016 Fiscal Year Final Research Report
The role of human CD161+gamma delta T cells in interstitial lung disease
Project/Area Number |
26461483
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Collagenous pathology/Allergology
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Research Institution | University of Tsukuba |
Principal Investigator |
GOTO Daisuke 筑波大学, 医学医療系, 准教授 (50344891)
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Research Collaborator |
SEGAWA Seiji
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | 間質性肺炎 / γδT細胞 / インターフェロンγ / インターロイキン17A |
Outline of Final Research Achievements |
I have reported the inflammatory role of γδ T cells that expressed NK1.1 in PBMCs in interstitial lung disease (ILD) mice models. In humans, mouse NK1.1 is homologous with CD161. The proportion of CD161+γδT cells was significantly higher in systemic sclerosis (SSc) than healthy controls (HCs) and correlated negatively with serum KL-6 levels in ILD-positive SSc patients. CD161+γδT cells in ILD-positive SSc patients showed lower production of IFN-γ than in HCs. These findings suggest that CD161+γδT cells may play a regulatory role in the pathogenesis of ILD in SSc patients via IFN-γ production. In bleomycin-induced ILD model mice, pulmonaryγδT cells were expanded and produced large amounts of IFN-γand IL-17A. Th17 cell differentiation was suppressed in the presence of IFN-γ producingγδT cells. These results suggested that pulmonaryγδT cells seem to play a regulatory role in the development of ILD via the suppression of IL-17A production.
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Free Research Field |
膠原病リウマチ学
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