2009 Fiscal Year Final Research Report
Analysis of signaling pathways induced by the binding of IL-1・to integrins
| Project/Area Number |
20890126
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| Research Category |
Grant-in-Aid for Young Scientists (Start-up)
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| Allocation Type | Single-year Grants |
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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 | Kobe University |
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Principal Investigator |
SAEGUSA Jun Kobe University, 大学院・医学研究科, 特命助教 (20514970)
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| Co-Investigator(Renkei-kenkyūsha) |
TAKADA Yoshikazu , カリフォルニア大学デービス校, 教授
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| Project Period (FY) |
2008 – 2009
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| Keywords | インターロイキン-1 / インテグリン / 関節リウマチ / サイトカイン / 滑膜細胞 |
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| Research Abstract |
Interleukin-1・(IL-1・) is a proinflammatory cytokine driving local as well as systemic inflammation by binding to its specific receptor, IL-1R type I, on target cells. In this study, we demonstrated that IL-1・・also specifically binds to integrin, which is known as a cell adhesion molecule. In addition, we showed that the integrin-binding site of IL-1・is distinct from the IL-1R-binding site using mutagenesis. Furthermore, we found that IL-1・・can activate MAP kinase pathway or NF-・B pathway in a manner independent of binding to IL-1R.
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[Journal Article] A T cell-binding fragment of fibrinogen can prevent autoimmunity.2010
Author(s)
Takada Y, Ono Y, Saegusa J, Mitsiades C, Mitsiades N, Tsai J, He Y, Maningding E, Coleman A, Ramirez-Maverakis D, Rodriquez R, Takada Y, Maverakis E.
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Journal Title
J Autoimmun. 34(4)
Pages: 453-9
Peer Reviewed
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