Roles of IL-5-producing ILC2 and eosinophil in IL-33-induced arterial hypertrophy
| Project/Area Number |
26860319
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Immunology
|
|---|
| Research Institution | University of Toyama |
|---|
Principal Investigator |
Ikutani Masashi 富山大学, 大学院医学薬学研究部(医学), 客員講師 (40513718)
|
|---|
| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | IL-5 / IL-33 / ILC2 / 好酸球 / Eosinophil / PAH |
|---|
| Outline of Final Research Achievements |
This study is aimed at clarifying the pathogenic mechanism (s) underlying pulmonary arterial hypertension (PAH). Previously, we developed an animal model of PAH. In the model, ILC2 and eosinophils were identified as the primary cause to develop PAH. These cells were accumulated around arterial blood vessels and this resulted in arterial hypertrophy. Involvement of these cells has not been reported and the findings from this study will lead to a new therapeutic approach.
|
Report
(3 results)
Research Products
(4 results)
