| Project/Area Number |
22591091
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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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 | Kyoto University |
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Principal Investigator |
FUJII Takao 京都大学, 医学研究科, 特定准教授 (70255462)
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| Co-Investigator(Kenkyū-buntansha) |
YUKAWA Naoichiro 京都大学, 医学研究科, 助教 (90422972)
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| Research Collaborator |
YUKAWA Naoichiro (90422972)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | タイプIインターフェロン / 抗核抗体 / 全身性エリテマトーデス / タイプI インターフェロン / 肺高血圧症 / 血管内皮細胞 / 中枢神経ループス / ケモカイン / インターフェロン-α / インターフェロン-β / 肺血管内皮細胞 / 肺微小血管内皮細胞 |
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| Research Abstract |
In the present study, I focused on neuropsychiatric systemic lupus erythematosus (NPSLE) and pulmonary arterial hypertension (PAH), which are associated with anti-U1 ribonucleoprotein antibodies (anti-U1RNP Abs). Type I IFN (IFN-α/β) could stimulates pulmonary arterial endothelial cells to secrete fractalkine and RANTES, that was suppressed by JAK inhibitors. In NPSLE, the presence of anti-U1RNP Abs in cerebrospinal fluid (CSF) was associated with high levels of IFN-α and MCP-1.
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