| Project/Area Number |
14370795
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Laboratory medicine
|
|---|
| Research Institution | Osaka University |
|---|
Principal Investigator |
IWATANI Yoshinori Osaka Univ., Osaka Univ. Graduate School of Medicine, Professor, 医学系研究科, 教授 (60168581)
|
|---|
| Project Period (FY) |
2002 – 2003
|
| Project Status |
Completed (Fiscal Year 2003)
|
| Budget Amount *help |
¥4,500,000 (Direct Cost: ¥4,500,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2002: ¥3,000,000 (Direct Cost: ¥3,000,000)
|
|---|
| Keywords | autoimmune / thyroid / deep vein thrombosis / CD25+CD4+ cells / CD25+CD8+ cells / CD50+CD8+ cells / IgG3-secreting cells / interleukin-10 (IL-10) / 予後診断法 / CD30 / CD4 / CD8 / IgG3 / IgA / CD25+CD4+細胞 / NKT細胞 / 樹状細胞 / CD30+CD8+細胞 |
|---|
| Research Abstract |
To develop the diagnostic method for the prognosis of autoimmune disease, we investigated various immunoregulatory cells and molecules which may determine the pathogenesis and the prognosis of autoimmune disease, and clarified as follows.
1.In autoimmune thyroid disease, the proportions of regulatory CD25+CD4+ cells and NKT cells were lower in thyroid than in blood, and there was a possibility that FasL+CD4+CD8+ dendritic cells may cause apoptosis of Fas+CD4+ cells in thyroid.
2.Activated cytotoxic T cells and thyroid autoantibodies were independently involved in the development of hypothyroidism in Hashimoto's disease and a decrease of CD30 expression on CD30+CD8+ cells was also involved in this development.
3.The number of IgG3-secreting cells and the level of IL-10 were involved in the intractability of Graves' disease under treatment with anti-thyroid drugs.
4.Acquired activated protein C resistance was associated with anti-protein S antibody as a strong risk factor for deep vein thrombosis in non-SLE patients, and was associated with the co-existence of anti-prothrombin antibodies and lupus anticoagulant activity in SLE patients.
|
