Project/Area Number |
15K08433
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Experimental pathology
|
Research Institution | Tokyo Medical University |
Principal Investigator |
Xu Mingli 東京医科大学, 医学部, 客員講師 (80597964)
|
Co-Investigator(Kenkyū-buntansha) |
善本 隆之 東京医科大学, 医学部, 教授 (80202406)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | EBI3 / p19 / heterodimeric cytokine / IL-27 / IL-23 |
Outline of Final Research Achievements |
In the present study, we elucidated that Epstein-Barr virus-induced gene 3 (EBI3), a common subunit of IL-27 and IL-35, and p19, one of IL-23 subunits can form a functional heterodimeric cytokine. EBI3 was first revealed to associate with p19, and subsequently hydrodynamic injection of the expression vector of a single chain of EBI3/p19 into mice was shown to augment an antigen-specific production of cytokines such as IL-17 and granulocyte-macrophage colony-stimulating factor in the draining lymph node cells. Then, transgenic mice over expressing the single chain of EBI3/p19 were established and exhibited resistance to the development of autoimmune hepatitis induced by injection with concanavalin A. Moreover, using a transplantable mouse tumor model of melanoma B16F10, EBI3/p19 was demonstrated to show potent antitumor activity. Currently, more detailed analysis on the molecular mechanism and its physiological role is under investigation.
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