| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Outline of Final Research Achievements |
CD11c-specific Shp-1 deficient mice (Shp1-CKO mice) spontaneously develop tubulointerstitial nephritis together with proliferative glomerulonephritis. In this study, we further examined the details of intrarenal immune-inflammatory cells in the kidney using flow cytometric analysis. CD11c (dendritic cell marker) and F4/80 (macrophage marker) double-positive renal mononuclear phagocytes were activated and increased in the kidney of Shp1-CKO mice. These renal mononuclear phagocytes are considered to induce accumulation of Th1 cells and possibly directly be involved in renal fibrosis. Our study showed that the mechanisms of tubulointerstitial injury and fibrosis via renal mononuclear phagocytes. In addition, Shp1 would play an important role in regulation of renal mononuclear phagocytes.
|
