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Search for Correlation of CD8 T Cell Response to Epstein-Barr Virus with Clinical Status in Rheumatoid Arthritis: A 15 Month Followup Pilot Study
JEAN-MARIE BERTHELOT, XAVIER SAULQUIN, MARIANNE COSTE-BUREL, MARIE A. PEYRAT, KLARA ECHASSERIEAU, MARC BONNEVILLE, and ELISABETH HOUSSAINT
ABSTRACT.
Methods. At each patient's visit every 3 months: (1) RA activity was assessed for Disease Activity Score (DAS-28); (2) a qualitative PCR for EBV was performed; (3) CD8 T cell response to EBV epitopes was screened in peripheral blood, using an autopresentation assay of 13 EBV peptides previously identified as immunodominant targets in RA synovia. Activation of anti-EBV CD8 T cells was evaluated by measuring the release of tumor necrosis factor-a. Results. The semiquantitative CD8 T cell response to EBV roughly paralleled RA clinical activity in only 4/17 patients. No clear association could be found between positive PCR for EBV (performed at least once in 10/17 patients) and RA activity/severity or fatigue. Reactivity was not qualitatively broader in samples where PCR for EBV proved positive, and most often focused on one or 2 EBV antigens. However, these antigens differed between patients, as did the magnitude of CD8 T cell response to immunodominant antigens at different timepoints for the same patient. Conclusion. The CD8 T cell response to EBV paralleled clinical activity in only 4/17 patients. Our pilot study does not support the hypothesis that this CD8 response contributes to RA activity/flares, although the quantitative variations in the pattern of this reactivity over time confirmed that control of EBV manifestations was difficult in most patients with RA. (J Rheumatol 2003;30:1673-9) Key Indexing Terms:
RHEUMATOID ARTHRITIS
From the Rheumatology Unit, CHU Nantes; INSERM U463, Institut de Biologie; and Laboratory of Virology, CHU Nantes, Nantes, France. Supported in part by the Association pour la Recherche sur la Polyarthrite (ARP), La Ligue Nationale contre le Cancer (LNCC), the Centre Hospitalier de Nantes, and by institutional grants from INSERM. J-M. Berthelot, MD, Rheumatology Unit, CHU Nantes; X. Saulquin, PhD; M.A. Peyrat; K. Echasserieau; M. Bonneville, PhD; E. Houssaint, PhD, INSERM U463, Institut de Biologie; M. Coste-Burel, MD, Laboratory of Virology, CHU Nantes. Address reprint requests to Dr. J-M. Berthelot, Service de Rhumatologie, Hôtel-Dieu, CHU Nantes, 44093, Nantes-Cedex 01, France. E-mail: jeanmarie.berthelot@chu-nantes.fr Submitted July 3, 2002; revision accepted January 8, 2003. |