The influence of a peptide sequence from PF-4 (CT-112) on type II collagen-induced arthritis in mice

Wooley, Paul H.; Whalen, Janey D.; Dutcher, Julie; Counts, David F.

doi:10.1007/bf01778294

Cited by 11 publications

(13 citation statements)

References 8 publications

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“…Chemokine antagonists have similarly shown promise. For instance, a 67-amino acid sequence of MCP-1 that specifically antagonizes MCP-1 abrogated arthritis in MRL-lpr autoimmune mice, and an antagonist of RANTES ameliorated CIA in mice (47)(48)(49). IL-1 receptor antagonist protein, a naturally produced specific antagonist of IL-1␤, has consistently shown potent antiinflammatory properties in animal models of inflammation (50)(51)(52) and is used in the treatment of RA (53)(54)(55)(56)(57)(58).…”

Section: Discussionmentioning

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

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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Section: Discussionmentioning

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

107

View full text Add to dashboard Cite

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“…An antiinflammatory peptide of PF-4/CXCL4 successfully inhibited mouse CIA when administered therapeutically (106). Although the mechanism of action of this peptide was unclear, interestingly, circulating IL-1 levels decreased with treatment.…”

Section: Chemokine Targeting Strategies In Experimental Arthritismentioning

confidence: 98%

“…PF-4/CXCL4 is angiostatic and inhibits endothelial cell proliferation (106). An antiinflammatory peptide of PF-4/CXCL4 successfully inhibited mouse CIA when administered therapeutically (106).…”

Section: Chemokine Targeting Strategies In Experimental Arthritismentioning

confidence: 99%

Chemokines and their receptors in rheumatoid arthritis: Future targets?

Koch¹

2005

Arthritis & Rheumatism

225

208

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“…Neutralizing Abs to CCL5 and naked DNA vaccines encoding CCL2, CCL3, CCL4, CCL5, and CXCL10 reduced the severity of AA (17)(18)(19). A CXCL4 octapeptide prevented development of disease in CIA (42). Met-RANTES, which inhibits CCR1 and CCR5 function, and two different nonpeptide CCR5 antagonists reduced the severity of CIA and reduced leukocyte accumulation assessed histologically (20 -22).…”

Section: Cxcr3 and Ccr5 Inmentioning

confidence: 99%

Blockade of Chemokine Receptor CXCR3 Inhibits T Cell Recruitment to Inflamed Joints and Decreases the Severity of Adjuvant Arthritis

Karkada

Issekutz

2007

The Journal of Immunology

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T lymphocytes expressing the chemokine receptors, CCR2, CCR5, CXCR3, and CXCR6 are increased in inflamed tissues in rheumatoid arthritis. The role of CXCR3 in autoimmune arthritis induced in Lewis rats was investigated. CXCR3+ T cells migrated 2- to 3-fold more than CXCR3− T cells to inflamed joints in arthritic animals. CXCR3-expressing in vivo Ag-activated T lymphoblasts and in vitro-activated lymph node cells from arthritic animals were strongly recruited to the arthritic joints, and treatment with anti-CXCR3 mAb significantly inhibited this T cell recruitment by 40–60%. Immune T cells from the spleen and lymph nodes of actively immunized arthritic donors adoptively transferred arthritis to naive rats. Treatment with anti-CXCR3 mAb delayed the onset of arthritis and significantly reduced the severity of joint inflammation with a >50% decrease in the clinical arthritis score. Blockade of CXCR3 also significantly reduced the weight loss in the arthritic animals and inhibited neutrophil accumulation in the joints by 50–60%. There was a marked reduction in the leukocyte infiltration of the synovium in the presence of CXCR3 blockade and a decrease in the loss of articular cartilage of the joints. In conclusion, CXCR3 on T cells has an essential role in T cell recruitment to inflamed joints and the development of joint inflammation in adjuvant arthritis.

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The influence of a peptide sequence from PF-4 (CT-112) on type II collagen-induced arthritis in mice

Cited by 11 publications

References 8 publications

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

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

Chemokines and their receptors in rheumatoid arthritis: Future targets?

Blockade of Chemokine Receptor CXCR3 Inhibits T Cell Recruitment to Inflamed Joints and Decreases the Severity of Adjuvant Arthritis

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