Project/Area Number |
15390313
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
膠原病・アレルギー・感染症内科学
|
Research Institution | KANAZAWA MEDICAL UNIVERSITY (2004-2005) Kyoto University (2003) |
Principal Investigator |
UMEHARA Hisanori Kanazawa Med. Univ, Dept.Hematol.Immunol, Prof, 医学部, 教授 (70247881)
|
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)
今井 俊夫 カン研究所, 所長
|
Project Period (FY) |
2003 – 2005
|
Project Status |
Completed (Fiscal Year 2005)
|
Budget Amount *help |
¥11,700,000 (Direct Cost: ¥11,700,000)
Fiscal Year 2005: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥4,500,000 (Direct Cost: ¥4,500,000)
|
Keywords | fractalkine / NK cell / cell adhesion / endothelial cell / IFN-γ / cellular damage / systemic sclerosis / フラクタルカン |
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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