| 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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| 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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