The analysis of new therapeutic targets involved in the progression of interstitial pneumonia
| Project/Area Number |
16K20932
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Collagenous pathology/Allergology
Respiratory organ internal medicine
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| Research Institution | University of Tsukuba |
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Principal Investigator |
Segawa Seiji 筑波大学, 医学医療系, 助教 (60632239)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 間質性肺炎 / γδT細胞 / Th17細胞 / Th17 / 免疫学 |
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| Outline of Final Research Achievements |
Interstitial pneumonia (IP) is a chronic progressive interstitial lung disease associated with poor prognosis and high mortality. However, the pathogenesis of IP remains to be elucidated. The aim of this study was to clarify the role of pulmonary γδT cells in IP.
In TCRδ deficient mice, bleomycin-induced IP was more severe than WT mice. And, pulmonary Th17 cells were more expanding in TCRδ deficient mice than in WT mice after bleomycin treatment. In vitro, Th17 cell differentiation was suppressed in the presence of IFN-γ producing γδT cells.Pulmonary fibrosis was attenuated by IFN-γ-producing γδT cells through the suppression of pulmonary Th17 cells.
These results suggested that pulmonary γδT cells seem to play a regulatory role in the development of bleomycin-induced IP mouse model via the suppression of IL-17A production.
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Report
(3 results)
Research Products
(2 results)
