| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
* Department of Medicine and Rheumatology, Graduate School,
Graduate School of Health Sciences, Tokyo Medical and Dental University, Tokyo, Japan;
KAN Research Institute, Kyoto, Japan; and
Eisai Co., Ltd., Ibaraki, Japan
Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with massive infiltration of inflammatory cells in the synovium of multiple joints. We and others have shown that fractalkine (FKN/CX3CL1), a chemokine expressed on fibroblast-like synoviocytes and endothelial cells in RA synovium, may contribute to the accumulation of T cells, macrophages, and dendritic cells, which express CX3CR1, the receptor for FKN. This interaction might be involved in adhesion of the inflammatory cells to endothelial cells, migration into the synovium, and cytokine production. In this study, we examined the effect of FKN inhibition on murine collagen-induced arthritis. Anti-FKN mAb significantly lowered clinical arthritis score compared with control Ab, and reduced infiltration of inflammatory cells and bone erosion in the synovium. However, anti-FKN mAb did not affect the production of either serum anti-collagen type II (CII) IgG or IFN-
by CII-stimulated splenic T cells. Furthermore, treatment with anti-FKN mAb inhibited migration of adoptively transferred splenic macrophages into the inflamed synovium. Our results suggest that anti-FKN mAb ameliorates arthritis by inhibiting infiltration of inflammatory cells into the synovium. Thus, FKN can be a new target molecule for the treatment of RA.
This article has been cited by other articles:
|
|
 |
|
  T. ODAI, M. MATSUNAWA, R. TAKAHASHI, K. WAKABAYASHI, T. ISOZAKI, N. YAJIMA, Y. MIWA, and T. KASAMA Correlation of CX3CL1 and CX3CR1 Levels with Response to Infliximab Therapy in Patients with Rheumatoid Arthritis J Rheumatol, June 1, 2009; 36(6): 1158 - 1165. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Montecucco and F. Mach Common inflammatory mediators orchestrate pathophysiological processes in rheumatoid arthritis and atherosclerosis Rheumatology, January 1, 2009; 48(1): 11 - 22. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Murphy, N. Caplice, and M. Molloy Fractalkine in rheumatoid arthritis: a review to date Rheumatology, October 1, 2008; 47(10): 1446 - 1451. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Kezic, H. Xu, H. R. Chinnery, C. C. Murphy, and P. G. McMenamin Retinal Microglia and Uveal Tract Dendritic Cells and Macrophages Are Not CX3CR1 Dependent in Their Recruitment and Distribution in the Young Mouse Eye Invest. Ophthalmol. Vis. Sci., April 1, 2008; 49(4): 1599 - 1608. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Lu, L. Li, K. Kuno, Y. Wu, T. Baba, Y.-y. Li, X. Zhang, and N. Mukaida Protective Roles of the Fractalkine/CX3CL1-CX3CR1 Interactions in Alkali-Induced Corneal Neovascularization through Enhanced Antiangiogenic Factor Expression J. Immunol., March 15, 2008; 180(6): 4283 - 4291. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Yamaguchi, K. Fujio, H. Shoda, A. Okamoto, N. H. Tsuno, K. Takahashi, and K. Yamamoto IL-17B and IL-17C Are Associated with TNF-{alpha} Production and Contribute to the Exacerbation of Inflammatory Arthritis J. Immunol., November 15, 2007; 179(10): 7128 - 7136. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S.-J. Lee, S. Namkoong, Y.-M. Kim, C.-K. Kim, H. Lee, K.-S. Ha, H.-T. Chung, Y.-G. Kwon, and Y.-M. Kim Fractalkine stimulates angiogenesis by activating the Raf-1/MEK/ERK- and PI3K/Akt/eNOS-dependent signal pathways Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H2836 - H2846. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S.-O. Moon, W. Kim, M. J. Sung, S. Lee, K. P. Kang, D. H. Kim, S. Y. Lee, J.-N. So, and S. K. Park Resveratrol Suppresses Tumor Necrosis Factor-{alpha}-Induced Fractalkine Expression in Endothelial Cells Mol. Pharmacol., July 1, 2006; 70(1): 112 - 119. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Suzuki, T. Nanki, T. Imai, H. Kikuchi, S. Hirohata, H. Kohsaka, and N. Miyasaka Inhibition of CX3CL1 (Fractalkine) Improves Experimental Autoimmune Myositis in SJL/J Mice J. Immunol., November 15, 2005; 175(10): 6987 - 6996. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-C. Gevrey, B. M. Isaac, and D. Cox Syk Is Required for Monocyte/Macrophage Chemotaxis to CX3CL1 (Fractalkine) J. Immunol., September 15, 2005; 175(6): 3737 - 3745. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
