| Project/Area Number |
08457151
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
内科学一般
|
|---|
| Research Institution | Tohoku University |
|---|
Principal Investigator |
SASAKI Takeshi Tohoku Univ.Sch.Med.Professor, 医学部, 教授 (50110656)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TAKAHASHI Yuichi Tohoku Univ.Sch.Med.Lecturer, 医学部・附属病院, 講師 (80261535)
SHIBATA Shinobu Tohoku Univ.Sch.Med.Research associate, 医学部・附属病院, 助手 (00271932)
FUNATO Tadao Tohoku Univ.Sch.Med.Lecturer., 医学部・附属病院, 講師 (70165455)
|
|---|
| Project Period (FY) |
1996 – 1997
|
| Project Status |
Completed (Fiscal Year 1997)
|
| Budget Amount *help |
¥7,800,000 (Direct Cost: ¥7,800,000)
Fiscal Year 1997: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1996: ¥5,800,000 (Direct Cost: ¥5,800,000)
|
|---|
| Keywords | human parvovirus / B19 / rheumatoid arthritis / arthritis |
|---|
| Research Abstract |
The etiology of rhumatoid arthritis (RA) is unknown. We have shown the persistence of human parvovirus B19 (B19) for more than 6 years in a patients with B19 infections and also the cases, who developed into active RA after an acute B19 infection. B19-DNA and the B19 antigen VP-1 were detected in the synovial tissues in 23 out of 30 patients with RA,and infrequently in those with osteoarthrits (OA) and traumatic joints. The expression of VP-1 was specific in active synoviaI lesions of RA.In situ hybridization and immunohistochemical studies revealed that the target cells of B19 were macrophages, foIIicular dendritic cells, T Cells and B cells, but not synoviaI lining cells in the snovium. B19-negative bone marrow cells, anc macrophage ceIls became positive for the expression of VP-1, and more productive for IL-6 and tumor necrosis factor alpha (TNF alpha) when cocultured with RA synovial cells. The expression of VP-1 and the production of IL-6 and TNF alpha was significantly inhibited by the addition of neutralizing antibody for B19, suggesting that B19 detected in RA synovial cells are infective. These data indicate that B19 may be involved in the initiation and perpetuation of RA synovitis, leading to joint lesions.
|
