| Project/Area Number |
26670240
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Immunology
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| Research Institution | Toho University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
KUWABARA Taku 東邦大学, 医学部, 講師 (40385563)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | Ｔ細胞 / ＳＡＴＢ１ / 自己免疫疾患 / SATB1 / 免疫寛容 / 自己免疫 |
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| Outline of Final Research Achievements |
Special AT-rich binding protein-1 (SATB1) is a chromosome organizer. Hematopoietic cell specific deletion of SATB1 in mice (SATB1cKO) leads to autoimmune manifestation; however, SATB1cKO mice were resistant against EAE. Spontaneous EAE with 2D2 transgenic TCR was not observed in SATB1cKO mice. Since TCR signal strength was weak in T cells from SATB1cKO mice, these results imply that T cells in SATB1cKO mice at childhood might play a role in pathogenesis of autoimmune diseases.
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