2014 Fiscal Year Final Research Report
How dendritic cell functional plasticity is maintained? an approach from TSLP signal transduction study
| Project/Area Number |
24591468
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | Saga University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
INOUE Hisako 前佐賀大学, 医学部, 助教 (10437816)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 樹状細胞 / 可塑性 / 細胞内シグナル伝達 / サイトカイン受容体 / TSLP / アレルギー |
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| Outline of Final Research Achievements |
Dendritic cells (DCs) have functional plasticity, by which distinct immune responses are induced depending on the nature of infection and inflammation. This phenomenon is granted by the fact that DCs can be differentially activated by distinct activating agents. DC activation through Toll-like receptors results in IL-12 production together with expression of IRF8 and STAT4, critical components of the IL-12 genes transcription. I found that type I interferon (IFN-beta) can induce IRF8 and STAT4 via ERK activation, where Th2-promoting activity of DCs that can be induced by TSLP is irreversibly lost. Thus, the type I IFN is suggested as the major factor that controls DC functional plasticity.
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| Free Research Field |
アレルギー学
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