2014 Fiscal Year Final Research Report
Regulation of chronic inflammatory disorders by Notch as a cell adhesion molecule
Project/Area Number |
25860295
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Experimental pathology
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Research Institution | Tottori University |
Principal Investigator |
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Project Period (FY) |
2013-04-01 – 2015-03-31
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Keywords | Notch / 接着分子 / 炎症性疾患 |
Outline of Final Research Achievements |
Notch ligands are known to be up-regulated in various inflammatory sites. However, the role of Notch in accumulation of immune cells is not clear. Here, we show that the Notch ligands (Delta-like 1 [Dll1], Dll4, Jagged1 and Jagged2) over-expressed in stromal cells markedly promote adhesion of various types of immune cells by functioning as cell adhesion molecules. Both Notch1 and Notch2 on immune cells are counter-receptors responsible for Notch ligands-mediated cell adhesion. These results suggest the possibility that Notch receptors and the ligands function as common adhesion molecules for immune cells. Therefore, cell adhesion mediated by Notch might be a therapeutic target for inhibiting recruitment of immune cells in inflammatory disorders.
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Free Research Field |
免疫学
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