2010 Fiscal Year Final Research Report
Role of a nuclear protein IκBζ in innate immunity
| Project/Area Number |
21790467
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | Osaka University |
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Principal Investigator |
YAMAMOTO Masahiro Osaka University, 医学系研究科, 准教授 (00444521)
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| Project Period (FY) |
2009 – 2010
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| Keywords | 原虫 / 自然免疫学 / 遺伝学 |
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| Research Abstract |
We clarified that an nuclear IκB family protein IκBζ is a master transcriptional factor for the generation of mouse Th17 cells. Ectopic co-expression of IκBζ and RORγt strongly induced Th17 differentiation even in the absence of IL-6 and TGF-β. In addition, IκBζ-deficient mice showed defective Th17 differentiation in vivo and resistance to EAE induction. Moreover, IκBζ in collaboration with RORγt directly associated with the promoter of IL17a and highly induced expression of IL17a.
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Research Products
(12 results)
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[Journal Article] NFATcl mediates Toll-like receptor-independent innate immune responses during Trypanosoma cruzi infection.2009
Author(s)
Kayama H, Koga R, Atarashi K, Okuyama M, Kimura T, Mak TW, Uematsu S, Akira S, Takayanagi H, Honda K, Yamamoto M, Takeda K.
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Journal Title
PLoS Pathog. 5
Pages: e1000514
Peer Reviewed
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[Journal Article] Involvement of linear polyubiquitylation of NEMO in NF-κB activation.2009
Author(s)
Tokunaga F, Sakata S, Saeki Y, Satomi Y, Kirisako T, Kamei K, Nakagawa T, Kato M, Murata S, Yamaoka S, Yamamoto M, et al
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Journal Title
Nat Cell Biol. 11
Pages: 123-32
Peer Reviewed
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