| Project/Area Number |
16K21285
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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
Medical pharmacy
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Fujii Chihiro 京都府立医科大学, 医学部附属病院, 研究員 (00516065)
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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: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 多発性硬化症 / フィンゴリモド / T細胞 / バイオマーカー / CD56陽性T細胞 / fingolimod / 細胞障害性分子 / IFN‐γ / MBP反応性T細胞 / IFN-γ / 疾患修飾薬 / 免疫学 |
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| Outline of Final Research Achievements |
We found that the frequency of CD56+ T cells in peripheral blood increased in fingolimod-treated patients with multiple sclerosis. These T cells expressed cytotoxic molecules and showed a Th1-like response. In addition, the CD56+ T cells produced IFN-γ in response to myelin basic protein. The elevated frequency of CD56+ T cells in fingolimod-treated patients was further increased at relapse. Relapse-experienced patients retained a higher frequency of CD56+ T cells even during remission compared to patients who did not have any relapse while on fingolimod treatment.
Our results showed that the T cell phenotypes were altered under fingolimod therapy,and raised a possibility that the frequency of CD56+ T cells is a useful biomarker for predicting and detecting relapses, although further confirmation is required.
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