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Expression and regulation of CCL18 in synovial fluid neutrophils of patients with rheumatoid arthritis.doc

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Expression and regulation of CCL18 in synovial fluid neutrophils of patients with rheumatoid arthritis

Available online /content/9/5/R94 Research article Open Access Vol 9 No 5 Expression and regulation of CCL18 in synovial fluid neutrophils of patients with rheumatoid arthritis Judith Auer1, Markus Bl?ss2, Hendrik Schulze-Koops3,4, Stefan Russwurm2,5, Thomas Nagel3, Joachim R Kalden3, Martin R?llinghoff1 and Horst Ulrich Beuscher1 1Institute for Clinical Microbiology, Immunology and Hygiene, University of Erlangen-Nuremberg, Wasserturmstrasse 3-5, D-91054 Erlangen, Germany 2SIRS-Lab GmbH, Winzerlaer Strasse 2, D-07745 Jena, Germany 3Department of Internal Medicine III and Institute for Clinical Immunology, Rheumatology and Onkology, University of Erlangen-Nuremberg, Krankenhausstrasse 12, D-91054 Erlangen, Germany 4Nikolaus Fiebiger Centre for Molecular Medicine, Clinical Research Group III, University of Erlangen-Nuremberg, Glücksstrasse 5, D-91054 Erlangen, Germany 5Clinics of Anesthesiology and Intensive Therapy, Friedrich-Schiller-University of Jena, Bachstrasse 18, D-07743 Jena, Germany Corresponding author: Horst Ulrich Beuscher, beuscher@mikrobio.med.uni-erlangen.de Received: 12 Feb 2007 Revisions requested: 22 Mar 2007 Revisions received: 17 Aug 2007 Accepted: 17 Sep 2007 Published: 17 Sep 2007 Arthritis Research Therapy 2007, 9:R94 (doi:10.1186/ar2294) This article is online at: /content/9/5/R94 ? 2007 Auer 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 Rheumatoid arthritis (RA) is characterized by the recruitment of leukocytes and the accumulation of inflammatory mediators within the synovial compartment. Release of the chemokine CCL18 has been widely attributed to antigen-presenting cells, receptor genes were differentially expressed, with upregulation of CXCR4, CCRL2 and CCR5 and downr