Dysregulated expression of MIG/CXCL9, IP-10/CXCL10 and CXCL16 and their receptors in systemic sclerosis |
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Authors: | Bradley J Rabquer Pei-Suen Tsou Yong Hou Eshwar Thirunavukkarasu G Kenneth Haines rd Ann J Impens Kristine Phillips Bashar Kahaleh James R Seibold Alisa E Koch |
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Affiliation: | (1) Department of Internal Medicine, University of Michigan Medical School, 109 Zina Pitcher Dr., Ann Arbor, MI 48109, USA;(2) Department of Pathology, Yale University, 200 South Frontage Rd., New Haven, CT 06510, USA;(3) Department of Medicine, University of Toledo, 3000 Arlington Ave., Toledo, OH 43614, USA;(4) Scleroderma Research Consultants, LLC, 97 Deer Run, Avon, CT 06001, USA;(5) Department of Veterans Affairs, VA Medical Service, 2215 Fuller Rd., Ann Arbor, MI 48105, USA |
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Abstract: | Introduction Systemic sclerosis (SSc) is characterized by fibrosis and microvascular abnormalities including dysregulated angiogenesis. Chemokines, in addition to their chemoattractant properties, have the ability to modulate angiogenesis. Chemokines lacking the enzyme-linked receptor (ELR) motif, such as monokine induced by interferon-γ (IFN-γ) (MIG/CXCL9) and IFN-inducible protein 10 (IP-10/CXCL10), inhibit angiogenesis by binding CXCR3. In addition, CXCL16 promotes angiogenesis by binding its unique receptor CXCR6. In this study, we determined the expression of these chemokines and receptors in SSc skin and serum. |
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