| Project/Area Number |
21790941
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | The University of Tokyo |
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Principal Investigator |
OKAMOTO Akiko The University of Tokyo, 医学部附属病院, 助教 (40431861)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 膠原病学 / 臨床免疫学 / 全身性エリテマトーデス / IL-17ファミリーサイトカイン / 内科学 / 脾臓貪食細胞 / 内科 / 自己免疫疾患 / サイトカイン |
|---|
| Research Abstract |
IL-17, a T cell-derived proinflammatory cytokine, contributes to the pathogenesis of rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). IL-17B and IL-17C belong to the IL-17 family. In our previous study, IL-17B is expressed in the cartilage and monocytes. IL-17C is expressed CD4^+Tcells, dendritic cells (DCs) and macrophages at the inflammatory site. IL-17B and IL-17C exacerbate and maintain inflammation in cooperate with Th17 cells or by themselves. In this study, IL-17B and IL-17C are expressed in the spleen (splenic DCs and macrophages) and kidney of lupus-prone NZB/W F_1 mice with nephritis. To examine the proinflammatory effects of IL-17B and IL-17C in vivo, adoptive transfer of IL-17B and IL-17C transduced CD4^+Tcells into NZB/WF1 is under examination. Assessments of modulation of phagocytosis and autoantigen-presentation capacity by IL-17B and IL-17C are in progress. Increase in IL-17B and IL-17C expression was not observed in PBMC from patients with SLE.
These ongoing experiments would clarify the pathogenic role of IL-17B and IL-17C in autoimmune disease.
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