| Project/Area Number |
02454195
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Immunology
|
|---|
| Research Institution | Juntendo University School of Medicine |
|---|
Principal Investigator |
YAGITA Hideo Juntendo University, School of Medicine, Associate Professor, 医学部, 助教授 (30182306)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
OKUMURA Ko Juntendo University, School of Medicine, Professor, 医学部, 教授 (50009700)
|
|---|
| Project Period (FY) |
1990 – 1992
|
| Project Status |
Completed (Fiscal Year 1992)
|
| Budget Amount *help |
¥6,200,000 (Direct Cost: ¥6,200,000)
Fiscal Year 1992: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1991: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1990: ¥3,600,000 (Direct Cost: ¥3,600,000)
|
|---|
| Keywords | adhesion molecules / extracellular matrix receptor / T cell activation / tolerance / integrins / CD4 / CD8 / CD2 / CD48 / LFA-1 / ICAM-1 / LFAー1 / ICAMー1 / T細胞分化 / CD_2 / CD11a / 18 / CD54 |
|---|
| Research Abstract |
(1)We revealed that CD4 and CD8 regulate IL-2 response of T cells via activation of p56^<lck> associated with them.
(2)We demonstrated that CD2-mediated signal plays an important role in T and NK cell activation.
(3)We revealed that CD48 is the predominant ligand for mouse CD2.
(4)We also demonstrated that CD48 is the second ligand for human CD2 other than LFA-3.
(5)We found that administration of anti-CD2 and anti-CD48 monoclonal antibodies led to a specific acceptance of mouse cardiac allografts.
(6)We found that administration of anti-LFA-1 and anti-ICAM-1 monoclonal antibodies led to a specific acceptance of mouse and rat cardiac allografts, which resulted from the induction of allospecific peripheral tolerance by clonal anergy. We also found that anti-VLA-4 and anti-VCAM-1 monoclonal antibodies had a similar effect although it was less efficient.
(7)We found that administration of anti-LFA-1 and anti-ICAM-1 monoclonal antibodies suppressed the pathogenesis of adjuvant arthritis in rats, collagen-induced arthritis in mice, and diabetes in NOD mice.
(8)We found that anti-VLA-4 and anti-VCAM-1 monoclonal antibodies specifically inhibited erythropoiesis in vitro and in vivo.
(9)We established monoclonal antibodies to mouse and rat vitronectin receptor, VLA-4, and VLA-5, and demonstrated that the interaction with fibronectin mediated by these integrins are critically involved in regulating T and mast cell activation.
(10)We established monoclonal antibodies to mouse VLA-1, VLA-2, VLA-3, and VLA-6, and examined the expression and function of these collagen and/or laminin receptors on hematopoietic cells.
(11)We revealed that beta_1 integrin-mediated interaction with extracellular matrix proteins regulates inflammatory cytokine gene expression in synovial fluid mononuclear cells of rheumatoid arthritis patients.
|
