| Project/Area Number |
26461468
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Collagenous pathology/Allergology
|
|---|
| Research Institution | Yokohama City University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
岳野 光洋 日本医科大学, 医学部, 准教授 (50236494)
上田 敦久 横浜市立大学, 医学研究科, 客員研究員 (60295483)
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Keywords | 膠原病学 |
|---|
| Outline of Final Research Achievements |
The up-regulation of type I interferon (IFN)-inducible genes, which is called “IFN signature”, is observed in several rheumatic diseases, such as systemic lupus erythematosus (SLE). In this study, we investigated the role of TRIM family proteins in the “IFN signature” using peripheral blood mononuclear cells (PBMC) from patients with the rheumatic diseases. Although the mRNA level of TRIM21 was significantly higher in PBMC from patients with SLE as compared to healthy controls (HC), proteasome-dependent degradation of IRF proteins, which are substrates of TRIM21, was impaired in SLE. The expression level of TRIM27 mRNA was significantly lower in PBMC from patients with SLE as compared to HC. The expression level of TBK1 protein, which is the substrate of TRIM27 and promotes type IFN production, was upregulated in SLE. These results suggest that dysregulation or dysfunction of TRIM family proteins leads to the overproduction of type I IFNs in SLE.
|
