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Abnormal Telomerase Activity and Telomere Length in T and B Cells from Patients with Systemic Lupus Erythematosus
DAITARO KUROSAKA, JUN YASUDA, KEN YOSHIDA, ASAKO YONEDA, CHIHO YASUDA, ISAMU KINGETSU, YASUHIKO TOYOKAWA, TORU YOKOYAMA, SABURO SAITO, and AKIO YAMADA ABSTRACT. Objective. To evaluate the clinical significance of telomerase activity and telomere length in T and B lymphocytes from patients with systemic lupus erythematosus (SLE). Methods. CD3+ (T cell) and CD19+ (B cell) lymphocytes were isolated from the peripheral blood of SLE patients and healthy controls by means of magnetic bead-coupled antibodies. SLE patients were classified as active or inactive cases according to the SLE Disease Activity Index (SLEDAI). Telomere activity of lymphocytes was measured by telomeric-repeat amplification protocol. Telomere length was measured by flow cytometry-fluorescence in situ hybridization. Results. T cell telomerase activity was significantly higher in patients with both active and inactive SLE than in controls, but was lower than B cell telomerase activity in patients with active SLE, and was not correlated with SLEDAI results. B cell telomerase activity was only significantly higher than in controls in patients with active SLE, and was strongly correlated with SLEDAI. Four laboratory results, anti-dsDNA antibody titer, IgG level, C3 level, and CH50 level, were correlated with B cell telomerase activity. Telomere length in T cells was significantly shorter than in controls. In contrast, the telomere length in B cells did not differ significantly from controls. Conclusion. In patients with SLE, many T cells divide continuously. Their telomerase activity was higher than that in control T cells, but not so high as to prevent telomere shortening. In contrast, B cells do not divide abnormally in the inactive phase of SLE, but divide rapidly in the active phase. (J Rheumatol 2006;33:1102–7) Key Indexing Terms:
TELOMERASE ACTIVITY
From the Division of Rheumatology, Department of Internal Medicine; and Department of Molecular Immunology, Institute of DNA Medicine, Jikei University School of Medicine, Tokyo, Japan. Supported by grants from Bio-Venture Research Fund Aid, Ministry of Education, Culture, Sports, Science and Technology of Japan. D. Kurosaka, MD, Assistant Professor; J. Yasuda, MD; K. Yoshida, MD; A. Yoneda; C. Yasuda, MD; I. Kingetsu, MD; Y. Toyokawa, MD; T. Yokoyama, MD; A. Yamada, MD, Professor, Division of Rheumatology, Department of Internal Medicine; S. Saito, MD, Associate Professor, Department of Molecular Immunology, Institute of DNA Medicine. Address reprint requests to Dr. D. Kurosaka, Division of Rheumatology, Department of Internal Medicine, Jikei University School of Medicine, 3-25-8, Nishishinbashi, Minato-ku, Tokyo, 105-8461, Japan. E-mail: d_kurosaka@jikei.ac.jp Accepted for publication January 13, 2006.
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