| Project/Area Number |
08839014
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
免疫の制御機構
|
|---|
| Research Institution | Osaka University |
|---|
Principal Investigator |
KOSUGI Atsushi Osaka University Medical School, Associate Professor, 医学部, 助教授 (90186685)
|
|---|
| Project Period (FY) |
1996 – 1997
|
| Project Status |
Completed (Fiscal Year 1997)
|
| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1997: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1996: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
|---|
| Keywords | T cells / T cell Receptor / TSA-1 / src-family kinases / DIG / CD3zeta / LCK / CD35鎖 / GPIアンカー型タン白質 / シグナル伝達 / 物理的会合 |
|---|
| Research Abstract |
Thymic shared antigen-1 (TSA-1)/stem cell Ag-2 (Sca-2) is a glycosyl-phosphatidylinositol (GPI) -anchored antigen expressed on lymphocytes. We have previously demonstrated that a signal via TSA-1/Sca-2 inhibits T cell receptor (TCR)-medialted T cell activation and apoptosis. To elucidate a molecular mechanism for TSA-1-mediated modulation of the TCR signaling pathway, we examined whether TSA-1 is physically coupled to the TCR in the present study. TSA-1 was clearly associated with CD3zeta chains in T cell hybridomas, activated T cells, and COS-7 cells transfected with TSA-1 and CD3zeta cDNA.The physical association was confirmed on the surface of T cells in immunoprecipitation and confocal microscopy. The analysis using stable and transient transfectants expressing a transmembrane form of TSA-1 revealed that the association of CD3zeta did not require the GPI anchor of TSA-1. Finally, tyrosine phosphorylation of CD3zeta chains was induced after stimulation with anti-TSA-1, suggesting that a functional association between these two molecules also exists. These results imply that the physical association to CD3zeta underlies a regulatory role of TSA-1/Sca-2 in TCR signaling pathway.
|
