Pro-inflammatory properties of stromal cell-derived factor-1 (CXCL12) in collagen-induced arthritis 英文参考文献.docVIP

Available online /content/7/6/R1208 Research article Open Access Vol 7 No 6 Pro-inflammatory properties of stromal cell-derived factor-1 (CXCL12) in collagen-induced arthritis Bert De Klerck1, Lies Geboes1, Sigrid Hatse2, Hilde Kelchtermans1, Yves Meyvis1, Kurt Vermeire2, Gary Bridger3, Alfons Billiau1, Dominique Schols2 and Patrick Matthys1 1Laboratory of Immunobiology, Rega Institute, Katholieke Universiteit Leuven, Leuven, Belgium 2Laboratory of Virology and Chemotherapy, Rega Institute, Katholieke Universiteit Leuven, Leuven, Belgium 3AnorMED, Langley, British Columbia, Canada Corresponding author: Bert De Klerck, bert.deklerck@rega.kuleuven.ac.be Received: 25 Mar 2005 Revisions requested: 9 May 2005 Revisions received: 14 Jul 2005 Accepted: 29 Jul 2005 Published: 25 Aug 2005 Arthritis Research Therapy 2005, 7:R1208-R1220 (DOI 10.1186/ar1806) This article is online at: /content/7/6/R1208 ? 2005 De Klerck et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/ 2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract CXCL12 (stromal cell-derived factor 1) is a unique biological ligand for the chemokine receptor CXCR4. We previously reported that treatment with a specific CXCR4 antagonist, AMD3100, exerts a beneficial effect on the development of collagen-induced arthritis (CIA) in the highly susceptible IFN-γ receptor-deficient (IFN-γR KO) mouse. We concluded that CXCL12 plays a central role in the pathogenesis of CIA in IFN- type II antibodies and, in contrast with its action in IFN-γR KO mice, did not inhibit the delayed type hypersensitivity response against collagen type II, suggesting that the beneficial effect cannot be explained by inhibition of humoral or cellular autoimmune responses. AMD3100 inhibited t