| Project/Area Number |
17K18263
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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
Immunology
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| Research Institution | Setsunan University |
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Principal Investigator |
Yoshida Yuya 摂南大学, 薬学部, 講師 (50581435)
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| Research Collaborator |
KOHNO Takeyuki 摂南大学, 薬学部, 教授 (50178224)
TSUJI Takumi 摂南大学, 薬学部, 准教授 (90454652)
BANNO Rie 摂南大学, 薬学部, 助教 (90736844)
MIKAMI Norihisa 大阪大学, 免疫学フロンティア研究センター・実験免疫学, 招へい教員 (20710388)
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2018: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | interleukin-10 / FTY720 / 免疫寛容 / 病因抗原 / 関節リウマチ / 寛解 / Interleukin-10 / フィンゴリモド |
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| Outline of Final Research Achievements |
Combination treatment with fingolimod (FTY720) and pathogenic antigen efficiently intduced immune tolerance to a mouse model of rheumatoid arthritis. In previous study, it has been suggested that GITR+ CD25- (or Foxp3-) CD4+ T cell populations, which are induced by this combination treatment and highly produce IL-10, may be involved in the induction of immune tolerance. In this study, the characteristics of this IL-10-producing T cell were examined. The cells showed low expression of CD45RA, CD62L, etc. and high expression of CD44, CD279 (PD-1), etc. Thus, it was revealed that they are a cell population having elements of effecter memory T cell and anergy.
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| Academic Significance and Societal Importance of the Research Achievements |
関節リウマチ等の自己免疫疾患に対して，長期間の寛解状態を誘導するには，病因リンパ球に対する免疫不応答の誘導が必須である．FTY720と病因抗原の併用治療は、病因リンパ球に対して，特異的かつ効果的に免疫不応答を導入できる可能性を秘めている．本申請課題では，治療効果発現の一角を担うと考えられる細胞集団の特性に関する情報が集積できた．本研究成果は，本併用治療による効果的な免疫寛容誘導機構の解明につながる重要な知見と考えられる．
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