FOXP3 isoform expression in the regulatory T cells in systemic lupus erythematosus patients and its role in the mechanism of the immue suppression
Project/Area Number |
19591177
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
膠原病・アレルギー・感染症内科学
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Research Institution | Saitama Medical University |
Principal Investigator |
SUZUKI Katsuya Saitama Medical University, 医学部, 助教 (70306695)
|
Co-Investigator(Kenkyū-buntansha) |
TAKEUCHI Tsutomu 埼玉医科大学, 医学部, 教授 (50179610)
|
Project Period (FY) |
2007 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2008: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2007: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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Keywords | 全身性エリテマトーデス / T細胞 / 制御性T細胞 / FOXP3 / アイソフォーム免疫寛容 / アイソフォーム / 免疫寛容 |
Research Abstract |
In patient with systemic lupus erythematosus (SLE), gene expression of both FOXP3 and its isoform, which express in regulatory T cell (Treg) that play an important role in immune tolerance, were decreased. These results indicated that both are important as a cause in immune tolerance in SLE. Next we investigated FOXP3 expression in immune suppressive state and found that decreased Treg subpopulation was not natural but induced Treg. From our study, we obtained important clues on the effective therapeutic target for SLE.
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Report
(4 results)
Research Products
(31 results)
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[Journal Article] IgG4-related systemic disease manifesting as Mikulicz disease with subsequent secondary portal hypertension and remarkable IgG4-linked IL-4 elevation2010
Author(s)
Suzuki K, Tamaru J, Okuyama A, Kameda H, Amano K, Nagasawa H, Nish E, Yoshimoto K, Setoyama Y, Kaneko K, Osada H, Honda N, Sasaki Y, Itoyama S, Tsuzaka K, Takeuchi T
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Journal Title
Related Report
Peer Reviewed
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