| Project/Area Number |
03670335
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
内科学一般
|
|---|
| Research Institution | Saitama Medical School |
|---|
Principal Investigator |
TAKEUCHI Tsutomu Saitama Medical Center Dep of Medicine, Asso.Prof., 医学部, 助教授 (50179610)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
AMANO Kohichi Saitama Medical Center Dep of Medicine, Assis.Prof., 医学部, 助手 (00175928)
KOIDE Jun Saitama Medical Center Dep of Medicine, Assis.Prof., 医学部, 講師 (70178193)
MATSUYAMA Takami Saitama Medical Center Dep of Medicine, Assis.Prof., 医学部, 教授 (30145479)
ABE Tohru Saitama Medical Center Dep of Medicine, Prof., 医学部, 教授 (60051207)
|
|---|
| Project Period (FY) |
1991 – 1992
|
| Project Status |
Completed (Fiscal Year 1992)
|
| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1992: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1991: ¥1,200,000 (Direct Cost: ¥1,200,000)
|
|---|
| Keywords | SLE / VLA-4 / LFA-1 / Lymphocytes / HUVEC / Vasculitis / VLAー4 / LFAー1 |
|---|
| Research Abstract |
Dysregulated expression of integrin adhesive receptors has implicated in various pathological conditions.We examined expression and function of integrins on peripheral blood lymphocytes from SLE,particularly those complicated by vasculitis. Here, we demonstrated that VLA-4 and LFA-l expression was increased in SLE patients with vasculitis, while LFA-l, but not VLA-4 expression was increased in those without vasculitis. These results suggested a role of VLA-4 in the pathogenesis of vasculitis in SLE. Functional studies further demonstrated that adhesion to cytokine-activated HUVECs and CS-1 alternatively spliced domain of fibronectin was significantly increased in SLE patients with vasculitis. Analysis for the functional epitopes on the alpha4 chain demonstrated that antigen densities of all the functional epitopes on alpha4 mere increased in those with vasculitis, indicating that the increased expression of VLA-4 was resulted from the increased amounts of VLA-4 molecules, but not secondary to increase in one particular functional epitope.
|
