| Project/Area Number |
02670285
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内科学一般
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| Research Institution | Nagasaki University |
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Principal Investigator |
EGUCHI Katsumi Nagasaki University School of Medicine, Lecturer, 医学部, 講師 (30128160)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Tatsufumi Nagasaki University School of Medicine, Assistant, 医学部, 助手 (00198219)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1991: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1990: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | HTLV-I / chronic inflammatory arthropathy / HTLV-I-infected T cell / synovial cell / HTLV-I pX gene / protooncogene / cytokine / transfection of gene / 抗HTLVーI抗体 / 合成HTLVーIエンベロップペプタイド / 血管内皮細胞 |
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| Research Abstract |
1. Infection of human synovial cells by human T-cell lymphotropic virus Type I : proliferation and granulocyte macrophage-colony stimulating factor production of synovial cells. To determine whether synovial cells are infected with HTLV-I and the infected synovial cells are able to proliferate actively and produce cytokines, the synovial cells were cocultured with HTLV-I-producing T cell lines. The synovial cells in the 5th passage after cocultivation with HTLV-I-producing T cells were shown to express the HTLV-L antigens by an immunohistochemical methods. The HTLV-I proviral DNA was also detected in the synovial cells by the polymerase chain reaction (PCR). The synovial cells by cocultivation with HTLV-I-infected T cell lines proliferate actively and transform. The proliferation of the synovial cells was essential to the contact with synovial cells and HTLV-I-producing T cell lines. Moreover, HTLV-I-infected synovial cells produced a significant amount of granulocyte macrophage-colony
… More
stimulating factor (GM-CSF). These results suggest that HTLV-l may cause chronic inflammetory arthropathy, as similar to that found in rheumatoid arthritis.
2. Transfection of HTLV-L pX gene into U937 cells.
U937 cells were transfected HTLV-L pX gene using DEAE dextran methods. U937 cells transfected HTLV-L pX gene was detected the pX MRNA by northern blotting and Tax protein by western blotting. A-IT-2 cells expressed the IL-2 Ra mRNA, but transfected U937 cells did not. However, the transfected U937 cells were detected c-fgr mRNA and p58^<c-fgr>.
3. Different B-cell responses to human T-cell lymphotropic virus Type I (HTLV-I) envelope synthetic peptides in HTLV-I-infected individuals.
We studied the difference in antibody activities against the viral protein and the difference in specificites of anti-HTLV-I envelope antibodies among HTLV-I-infected individuals from the same HTLV-I endemic area using a HTLV-I-gag hybrid protein and HTLV-I-env-encoded synthetic peptides as antigens, respectively. Patients with HTLV-I-infected polyarthritis made antibodies specific for VlE1 (residues 342-363) and VIE8 (191-209). Patients with HTLV-I associated myelopathy (HAM) made antibodies to the VIE7 (97-111) and VIE9 (268-286) epitopes. The activities of anti-HTLV-I antibodies in sera from HTLV-I-infected polyarthritis patients were not different from the activities of the antibodies from normal HTLV-I-carries, and no envelope peptide-specificity unique for the arthritis patients was detected. Less
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