| Project/Area Number |
10307012
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
内科学一般
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| Research Institution | Tohoku University |
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Principal Investigator |
SASAKI Takeshi Tohoku Univ., Graduated Sch. Med., Professor, 大学院・医学系研究科, 教授 (50110656)
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| Co-Investigator(Kenkyū-buntansha) |
FUNATO Tadao Tohoku Univ., Graduate School of Med., Lecture, 大学院・医学系研究科, 講師 (70165455)
SHIBATA Shinobu Tohoku Univ., Hospital, Research Associate, 医学部附属病院, 助手 (00271932)
MUNAKATA Yasuhiko Tohoku Univ., Hospital, Research Associate, 医学部附属病院, 助手 (20271950)
KAMEOKA Junichi Tohoku Univ., Hospital, Research Associate, 医学部附属病院, 助手 (30261621)
ISHII Keiko Tohoku Univ., Hospital, Lecture, 医学部附属病院, 講師 (00291253)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥32,500,000 (Direct Cost: ¥32,500,000)
Fiscal Year 2000: ¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1999: ¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1998: ¥27,000,000 (Direct Cost: ¥27,000,000)
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| Keywords | Rheumatoid arthritis / human parvorirus B19 / TNFα / macrophage / ヒトパルボウイルス / B19 / リボザイム |
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| Research Abstract |
1.We characterized DNA sequence of human parvovirus B19(B19) isolated from synovium tissues of 6 patients with rheumatoid arthritis. The results revealed no specific regions in B19 DNA derived from RA, compared with those from fifth desease.
2.We evaluated neutralizing ability of B19 antibody in humans. Anti-B19 antibodies from patients with fifth disease showed above 70% of inhibition on the increase of B19 DNA in B19-infected erythroid cell lines, whereas some from RA had significantly decreased inhibition of B19 increase, indicating that RA patients might permit persistent B19 infection in vivo.
3.B19 can proliferate not only in erythroid cells but also in immunocytes. We found a novel receptor for B19 which is different from P antigens in erythrocytes. The B19 infection to T cells caused an enhanced chomotaxic ability.
4.We established NS-1-transfected macrophage cell line, U937-NS1. The addition of IPTG induced an enhanced production of TNFαmRNA and NS1 mRNA, indicating that NS1 of B19 may be responsible for the production of TNFα in immunocytes invading rheumatoid synovium. We are investigating precise mechanism of molecular mechanism of TNFα production evoked by the activation of NS1 gene.
5.We obtained NS1 transgenic C57/B6(NS1Tg) mice. NS1 Tg mice showed a feasibility of type II collagen-induced polyarthritis.
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