2022 Fiscal Year Final Research Report
The role of IFN signature in the pathogenesis of human T-cell leukemia virus type 1-positive rheumatoid arthritis.
Project/Area Number |
20K08776
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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 |
Review Section |
Basic Section 54020:Connective tissue disease and allergy-related
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Research Institution | University of Miyazaki |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
佐藤 賢文 熊本大学, ヒトレトロウイルス学共同研究センター, 教授 (70402807)
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | ヒトT細胞白血病ウイルス / 関節リウマチ |
Outline of Final Research Achievements |
Human T-cell leukemia virus type 1 (HTLV-1) infection is known to modify the pathogenesis of rheumatoid arthritis (RA), such as exacerbation of inflammatory responses and inadequate response to anti-rheumatic therapies. As a factor, we are focusing on the mechanism of exacerbation of inflammatory process mediated by IFNγ in HTLV-1 positive RA. In this study, assuming that HTLV-1-positive RA has an "IFN signature", we identified IFNγ autonomously producing cells, analyzed the dynamics of HTLV-1-infected cells under immunosuppressive therapy, and investigated the association between disease activity of HTLV-1-positive RA and HTLV-1-infected cells or IFNγ autonomously producing cells.
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Free Research Field |
膠原病リウマチ性疾患
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Academic Significance and Societal Importance of the Research Achievements |
HTLV-1陽性関節リウマチ(RA)におけるIFNシグネチャーについて解析を進め,難治性病態であるHTLV-1陽性RAの病態について理解を深めた.具体的には,HTLV-1陽性RAの末梢血単核球におけるIFNγ自律産生細胞を同定した.この細胞集団は,HTLV-1感染細胞に対する抗ウイルス作用を有する細胞集団である可能性が高いと考えられたが,HTLV-1陽性RAの炎症病態においても何らかの役割を担うものと推察される.これらの知見から,今後のHTLV-1陽性RA患者のRA治療戦略において,IFNシグネチャーを軸にした抗リウマチ薬の選択について,その有効性や安全性などの検討が進むと考えられる.
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