Development of simulation method of cell group population based on signal transduction pathway's behaviors
| Project/Area Number |
20500275
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Bioinformatics/Life informatics
|
|---|
| Research Institution | Okayama University of Science |
|---|
Principal Investigator |
YAMADA Satoshi Okayama University of Science, 工学部, 教授 (20393506)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
YOSHIMURA Akihiko 慶應義塾大学, 医学部, 教授 (90182815)
|
|---|
| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Keywords | ヘルパーT細胞 / 免疫ネットワーク / 転写因子 / サイトカイン / シミュレーション / iTreg / Th17 |
|---|
| Research Abstract |
The computer model which simultaneously calculates intra-cellular reactions and population of cell groups was developed by constructing a model of the helper T cell differentiation. The model contained the interactions among transcription factors in Th0 and simple interactions among subtypes through cytokines. This model mimicked TCR-stimulation strength dependency and TGF-β dependency of Th17 and iTreg. To simulate such behaviors, an unknown inhibitory factor, which is induced by Foxp3 and inhibits RORγt actions, is required. The physiological role of iTreg was analyzed by the simulation of the system containing dendritic cells and nTreg.
|
Report
(4 results)
Research Products
(14 results)
