Fractalkine, a novel chemokine in rheumatoid arthritis and in rat adjuvant-induced arthritis

Ruth, Jeffrey H.; Volin, Michael V.; Haines, G. Kenneth; Woodruff, Drew C.; Katschke, Kenneth J.; Woods, James M.; Park, Christy C.; Morel, Jacques; Koch, Alisa E.

doi:10.1002/1529-0131(200107)44:7<1568::aid-art280>3.0.co;2-1

Cited by 225 publications

(206 citation statements)

References 43 publications

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“…However, it is the membrane-bound form that has generated the most interest as it potentially combines the direct action of an adhesion molecule with the specificity of a chemokine. Membrane-bound fractalkine is highly expressed in a number of murine models of inflammatory disease including cardiac allograft rejection [19], crescentric glomerulonephritis [20], and experimental autoimmune encephalomyelitis [21,22], as well as in the human inflammatory diseases rheumatoid arthritis [23], psoriasis [24] and atherosclerosis [25]. It is therefore very important to understand the mechanisms by which this chemokine may contribute to disease processes.…”

Section: Introductionmentioning

confidence: 99%

Human fractalkine mediates leukocyte adhesion but not capture under physiological shear conditions; a mechanism for selective monocyte recruitment

et al. 2003

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Fractalkine is a unique chemokine possessing a long mucin-like stalk and a transmembrane region that has been proposed to act as an adhesion molecule. We investigated the ability of fractalkine to recruit leukocytes from whole blood, using an immobilized fractalkine fusion protein in the parallel-plate flow-chamber assay. Significant adhesion of leukocytes to fractalkine peaked at 2 dynes/cm 2 but was minimal at 10 dynes/cm 2 . In contrast, VCAM-1 could recruit cells from whole blood at 10 dynes/cm 2 . Co-immobilization of fractalkine and VCAM-1 at 10 dynes/cm 2 resulted in a twofold increase in adherent cells compared with VCAM-1 alone, suggesting that fractalkine can mediate adhesion at high shear if combined with a molecule that can mediate leukocyte tethering. Pretreatment of blood with pertussis toxin eliminated this increase in adhesion, implicating intracellular signaling in fractalkinemediated mechanisms of adhesion to co-immobilized fractalkine/VCAM-1. Analysis of the cell types recruited to fractalkine alone at low shear, or to fractalkine and VCAM-1 at 10 dynes/cm 2 , revealed that monocytes were recruited to fractalkine with the highest specificity. In conclusion, fractalkine is unlikely to act alone at shear forces found in most vascular beds where it most likely co-operates with tethering molecules, e.g. VCAM-1, in the recruitment of monocytes.

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Section: Introductionmentioning

confidence: 99%

Human fractalkine mediates leukocyte adhesion but not capture under physiological shear conditions; a mechanism for selective monocyte recruitment

et al. 2003

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“…A number of cell-derived factors facilitate this process, including macrophage inflammatory protein 3␣ (MIP-3␣), granulocyte-macrophage colonystimulating factor, monocyte chemoattractant protein 1 (MCP-1), MIP-1␣, epithelial neutrophil-activating peptide 78 (ENA-78), fractalkine, and others (1)(2)(3)(4)(5)(6). Thera-pies designed to block the activity or inhibit the production of these mediators and their corresponding receptors are currently being developed.…”

mentioning

confidence: 99%

“…Finally, CXCL16 has a unique receptor-ligand interaction, much like fractalkine (24)(25)(26). These characteristics are important, considering the proinflammatory functions of fractalkine in RA and in rat adjuvant-induced arthritis (AIA) (3,4). Thus, the similar physical properties of fractalkine and CXCL16 are likely to result in similar proinflammatory activity.…”

mentioning

confidence: 99%

CXCL16‐mediated cell recruitment to rheumatoid arthritis synovial tissue and murine lymph nodes is dependent upon the MAPK pathway

Ruth¹,

Haas²,

Park³

et al. 2006

Arthritis & Rheumatism

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107

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Objective. Rheumatoid arthritis (RA) is characterized by profound mononuclear cell (MNC) recruitment into synovial tissue (ST), thought to be due in part to tumor necrosis factor ␣ (TNF␣), a therapeutic target for RA. Although chemokines may also be involved, the mechanisms remain unclear. We undertook this study to examine the participation of CXCL16, a novel chemokine, in recruitment of MNCs to RA ST in vivo and to determine the signal transduction pathways mediating this process. Conclusion. Taken together, these results point to a unique role for CXCL16 as a premier MNC recruiter in RA and suggest additional therapeutic possibilities, targeting CXCL16, its receptor, or its signaling pathways.

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“…The relevance of FKN as a fibroblast growth factor was confirmed in experiments testing the growth-promoting effect of exogenous FKN. A proinflammatory role for this chemokine has been supported by gene expression experiments in rat adjuvant-induced arthritis (22). FKN and its receptor CX 3 CR1 were abundantly expressed on day 18, a time of intense inflammation in the rat joint.…”

Section: Discussionmentioning

confidence: 92%

“…It has been proposed that FKN promotes recruitment of monocytes and T cells into the rheumatoid synovium (22)(23)(24). Recent work by our group suggests that in RA, the role of FKN extends beyond chemoattraction and adhesion (18).…”

mentioning

confidence: 95%

Fractalkine mediates T cell–dependent proliferation of synovial fibroblasts in rheumatoid arthritis

Sawai¹,

Park²,

He³

et al. 2007

Arthritis & Rheumatism

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Fractalkine, a novel chemokine in rheumatoid arthritis and in rat adjuvant-induced arthritis

Cited by 225 publications

References 43 publications

Human fractalkine mediates leukocyte adhesion but not capture under physiological shear conditions; a mechanism for selective monocyte recruitment

Human fractalkine mediates leukocyte adhesion but not capture under physiological shear conditions; a mechanism for selective monocyte recruitment

CXCL16‐mediated cell recruitment to rheumatoid arthritis synovial tissue and murine lymph nodes is dependent upon the MAPK pathway

Fractalkine mediates T cell–dependent proliferation of synovial fibroblasts in rheumatoid arthritis

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