| Project/Area Number |
25461615
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Pediatrics
|
|---|
| Research Institution | Hirosaki University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
IMAIZUMI TADAATSU 弘前大学, 大学院医学研究科, 教授 (90232602)
YOSHIDA HIDEMI 弘前大学, 大学院医学研究科, 講師 (40201008)
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
|---|
| Keywords | 腎炎症候群 / 自然免疫 / メサンギウム細胞 / 炎症性ケモカイン / Toll-like receptor 3 / ISG15 / Interferon-β / CXCL1 / TLR3 / human mesangial cells / pseudoviral immunity / lupus nephritis / toll-like receptor 3 / Mx1 / MCP-1 / CCL5 / mizoribine |
|---|
| Outline of Final Research Achievements |
Since viral infections activate type I interferon (IFN) pathways and cause subsequent release of IFN-dependent proinflammatory chemokines/cytokines, the innate immune system plays an important role in the pathogenesis of
glomerulonephritis (GN). So far, we have examined the toll-like receptor (TLR) 3 signaling cascades treated with polyinosinic-polycytidylic acid (poly IC), a synthetic analogue of viral dsRNA, that makes “pseudoviral” infection in cultured human mesangial cells (MCs). We found that the activation of mesangial TLR3 upregulated the expression of functional molecules acting as monocyte/macrophage and lymphocyte chemoattractants in MCs. Further, intense glomerular expressions of these functional molecules were observed in biopsy specimens from children with GN. These observations further support the implication of “pseudoviral” immunity in the pathogenesis of GN.
|
