| Project/Area Number |
23591443
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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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 | Yokohama City University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIMI Ryusuke 横浜市立大学, 医学部, 助教 (70585265)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | ベーチェット病 / ヘムオキシゲナーゼ-1 / IL-10 / 自己免疫 / 自己炎症 / HLA-クラスI / ERAP-1 / TLR4 / HLA-クラス I / HO-1 / 腫瘍壊死因子 |
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| Research Abstract |
In this study, we try to verify the hypothesis that impaired protective function by IL-10/HO-1 trigger autoimmune and autoinflammatory responses, leading to Behcet disease (BD). Further analyses after GWAS have identified CCR1, STAT4, KLRC4, ERAP1, TLR4, NOD2, and MEFV as susceptible genes, all of which are involved in the acquired and innate immunity systems. Of them, genetic contribution of TLR4 is concordant with our previous finding that overexpression of TLR4 is associated with defective expression of HO-1 in BD patients, suggesting validity of the hypothesis in part. Moreover, recent studies have shown that HO-1 is preferentially expressed on non-classical M2 macrophages, suggesting M1 deviation of M1/M2 balance is responsible for development of BD. The issue will be studied in the next grant (No. 26461469).
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