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Membrane Glucocorticoid Receptor Expression on Peripheral Blood Mononuclear Cells in Patients with Ankylosing Spondylitis
ANITA B. TRYC, CORNELIA M. SPIES, UDO SCHNEIDER, DESIREE KUNKEL, TIMEA BERKI, JOACHIM SIEPER, GERD-RÜDIGER BURMESTER, ANDREAS RADBRUCH, ALEXANDER SCHEFFOLD, and FRANK BUTTGEREIT ABSTRACT. Objective. To investigate the expression of membrane glucocorticoid receptors (mGCR) on peripheral blood mononuclear cells (PBMC) in patients with ankylosing spondylitis (AS). Methods. We used high sensitivity immunofluorescence with magnetofluorescent liposomes for the detection of mGCR on PBMC from patients with AS (n = 26) and healthy controls (n = 11). Results. The frequency of mGCR+ monocytes and B lymphocytes was significantly higher in patients with AS than in controls (monocytes 12.5 ± 9.9% vs 4.8 ± 1.4%, B lymphocytes 8.7 ± 6.3% vs 4.4 ± 3.6%). We did not find mGCR on T lymphocytes. The frequency of mGCR+ cells did not correlate with variables of AS disease activity [C-reactive protein, erythrocyte sedimentation rate, Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), BASDAI 6, or numerical rating scales]. Conclusion. mGCR are upregulated in monocytes and B lymphocytes of patients with AS. This upregulation does not correlate with the humoral or overall disease activity. mGCR are not present on T lymphocytes. Our findings may be related to the limited benefit of low-dose and the efficacy of high-dose (intravenous pulse or intraarticular) glucocorticoid treatment in AS. Drugs binding selectively to mGCR may be a new therapeutic option for AS. (First Release Sept 1 2006; J Rheumatol 2006;33:2249-53) Key Indexing Terms:
GLUCOCORTICOID From the Department of Rheumatology and Clinical Immunology, Charité University Hospital, Campus Mitte; the Medical Department, Rheumatology, Charité University Hospital, Campus Benjamin Franklin; and the German Arthritis Research Centre (DRFZ), Berlin, Germany; and from the Department of Immunology and Biotechnology, University of Pécs, Faculty of Medicine, Pécs, Hungary. Supported by grants from the Deutsche Forschungsgemeinschaft (Bu 1015/1-1, Bu 1015/4-1). A.B. Tryc; C.M. Spies, MD; U. Schneider, MD; F. Buttgereit, MD, Professor; G.R. Burmester, MD, Professor, Department of Rheumatology and Clinical Immunology, Charité University Hospital, Campus Mitte; J. Sieper, MD, Professor, Medical Department, Rheumatology, Charité University Hospital, Campus Benjamin Franklin; D. Kunkel, PhD; A. Scheffold, PhD; A. Radbruch, PhD, Professor, German Arthritis Research Centre (DRFZ); T. Berki, PhD, Department of Immunology and Biotechnology, University of Pécs. Address reprint requests to Dr. C.M. Spies, Department of Rheumatology and Clinical Immunology, Charité University Hospital, Campus Mitte, Charitéplatz 1, 10117 Berlin, Germany. E-mail: cornelia.spies@charite.de Accepted for publication May 29, 2006.
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