Development of autoimmune mouse model by viral factors
| Project/Area Number |
22300140
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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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 |
¥17,810,000 (Direct Cost: ¥13,700,000、Indirect Cost: ¥4,110,000)
Fiscal Year 2012: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2011: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2010: ¥6,760,000 (Direct Cost: ¥5,200,000、Indirect Cost: ¥1,560,000)
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| Keywords | パルボウイルス / NS / Bmper / DNA メチル化 / コラーゲン関節炎 / マウス / ＮＳ / アポトーシス / メチル化 / リンパ球 / BMPER / 自己免疫 / エピジェネシス / 自己免疫病 / 疾患モデル |
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| Research Abstract |
In the present study, it was elucidated that parvoviral nonstructure (NS) protein induced DNA methylation in T lymphocytes and caused change of apoptosis resistancy and cell proliferation. Moreover, a possible effect of NS for incidence of collagen-induced arthritis was examined in vivo. The most of mouse T lymphocytes infected with NS-EGFP expression vector caused apoptosis, and the survived cells suppressed Bmper expression by DNA methylation. These cells acquired to be resistant for parvoviral re-infection. DBA/1 mice infected with NS-EGFP expression vector developed collagen-induced arthritis, though there was no significant difference on incidence of them to that of the control.
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Report
(4 results)
Research Products
(7 results)
