2005 Fiscal Year Final Research Report Summary
The roles of fractalkine in pathogenesis of systemic sclerosis
| Project/Area Number |
15390313
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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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 | KANAZAWA MEDICAL UNIVERSITY (2004-2005)
Kyoto University (2003) |
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Principal Investigator |
UMEHARA Hisanori Kanazawa Med. Univ, Dept.Hematol.Immunol, Prof, 医学部, 教授 (70247881)
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| Co-Investigator(Kenkyū-buntansha) |
MIMORI Tsuneyo Kyoto Univ, Grad.Sch.Med.Clin.Immunol, Prof, 医学研究科, 教授 (10157589)
OGAWA Noriyoshi Kanazawa Med.Univ., Dept.Hematol.Immunol, Assoc.Prof, 医学部, 助教授 (80308618)
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| Project Period (FY) |
2003 – 2005
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| Keywords | fractalkine / NK cell / cell adhesion / endothelial cell / IFN-γ / cellular damage / systemic sclerosis |
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| Research Abstract |
Leukocyte adhesion and trafficking at the endothelium requires both adhesion molecules and chemotactic factors. Fractalkine (CX3C) is a unique chemokine, and expressed on TNF-α- and IL-1-activated endothelial cells (ECs). Fractalkine receptor, CX3CR1, is expressed on NK cells, monocytes and some portion of CD4- and CD8-positive T cells. Interactions between fractalkine and CX3CR1 can mediate not only chemotaxis, but also cell adhesion in the absence of substrates for other adhesion molecules. Furthermore, fractalkine activates NK cells, leading to increased cytotoxicity and IFN-γ production. Recently, accumulating evidence has shown that fractalkine is involved in the pathogenesis of rheumatoid arthritis and allied conditions. This review will examine new concepts underlying fractalkine-mediated leukocyte migration and tissue damage, focusing primarily on the pathophysiological roles of fractalkine in rheumatic diseases.
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Research Products
(17 results)
