| Project/Area Number |
18K08147
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 53030:Respiratory medicine-related
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| Research Institution | Oita University |
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Principal Investigator |
Ando Masaru 大分大学, 医学部, 客員研究員 (20336267)
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| Project Period (FY) |
2018-04-01 – 2024-03-31
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| Project Status |
Completed (Fiscal Year 2023)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | サルコイドーシス / 制御性T細胞 / サルコイドーシス重症度 / サルコイドーシス予後 / 免疫寛容 / 制御性Ｔ細胞 |
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| Outline of Final Research Achievements |
We examined the mechanisms of the serum and bronchoalveolar lavage fluid levels of cytokines and soluble cell markers to elucidate the mechanisms underlying the improvement in patients with sarcoidosis. The serum levels of Foxp3, which is considered to be a cell marker of regulatory T cells did not differ between the improvement group and the other group (no change/exacerbation/treatment with prednisolone). Weak correlation was observed between the serum levels of Foxp3 and BALF CCL20, and between Foxp3 and serum CCR6. When the improvement/no change and exacerbation/treatment groups were compared, the serum levels of CCL20, ACE, lysozyme and sIL-2R were higher in the exacerbation/treatment group. Thus, CCL20 may be a new surrogate biomarker for predict disease severity in patients with sarcoidosis.
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| Academic Significance and Societal Importance of the Research Achievements |
サルコイドーシスは、自然に改善するものから、ステロイドや免疫抑制剤を必要とする難治性のものまで病勢が多彩である。肉芽腫形成を抑制する機序として制御性T細胞の関与があるものと仮説をたてた。本研究では制御性T細胞の細胞マーカーsFOXP-3の発現は改善群とその他の群で有意差がみられなかった。今回の検討では明らかにできなかったが、制御性T細胞及びその細胞が関与する分子が肉芽腫の退縮機序に関与することが明らかになれば、難治性サルコイドーシスの新たな治療法の開発の一助となる。
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