Pathogenesis of biliary atresia-Interaction between biliary innate immunity and acquired immunity-
| Project/Area Number |
20590338
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Human pathology
|
|---|
| Research Institution | Kanazawa University |
|---|
Principal Investigator |
HARADA Kenichi Kanazawa University, 医学系, 准教授 (30283112)
|
|---|
| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2008: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
|---|
| Keywords | 胆道閉鎖症 / 胆管 / 自然免疫 / 病理学 / ウイルス / NK細胞 / 上皮間葉移行 / 獲得免疫 / 自己抗体 / EMT |
|---|
| Research Abstract |
Biliary innate immunity for double-stranded RNA virus was examined in the histopathogenesis of biliary atresia (BA). Epithelial-mesenchymal transition (EMT) of biliary epithelial cells induced by the stimulation with double-stranded RNA and EMT-like phenotypic changes of extrahepatic bile ducts in BA are closely associated with the histogenesis of sclerosing obliterative cholangitis. Moreover, the increased number of an unique subset of NK cells, CD56^-CD16^+NK cells was found in portal tracts of BA, suggesting that NK dysfunction against virus infection might be a host factor associated with pathogenesis of BA.
|
Report
(4 results)
Research Products
(41 results)
