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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Project Status |
Completed (Fiscal Year 2016)
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Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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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 / IFN-γ / IL-17A / CD161 / 強皮症 / CCL-3 |
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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Report
(4 results)
Research Products
(9 results)
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[Journal Article] Involvement of CD161+Vδ1+γδT cells in systemic sclerosis: association with interstitial pneumonia2014
Author(s)
Segawa S, Goto D, Horikoshi M, Kondo Y, Umeda N, Hagiwara S, Yokosawa M, Hirota T, Miki H, Tsuboi H, Ogishima H, Suzuki T, Matumoto I, Sumida T
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Journal Title
Rheumatology
Volume: 53
Pages: 2259-2269
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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