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Decreased Recent Thymus Emigrant Number Is Associated with Disease Activity in Systemic Lupus Erythematosus

QUEILA F. VIEIRA, CRISTIANE KAYSER, ESPER G. KALLAS, and LUÍS EDUARDO C. ANDRADE

ABSTRACT.

Objective.
T cell receptor excision circle (TREC) is produced during T cell maturation within the thymus, and the number of TREC-bearing cells reflects the proportion of recent thymic emigrants in the peripheral lymphocyte pool. We studied TREC levels in peripheral CD4+ and CD8+ lymphocytes in patients with systemic lupus erythematosus (SLE) with quiescent and with active disease and in age- and sex-matched healthy volunteers.

Methods. TREC levels in peripheral CD4+ and CD8+ lymphocytes were determined in 29 patients with quiescent SLE, in 22 with active disease, and in 31 age- and sex-matched healthy volunteers. The number of TREC/µg DNA was determined by real-time polymerase chain reaction gauged by a standard curve with known number of TREC-containing plasmids.

Results. TREC levels in CD4+ and CD8+ cells were lower in patients with active SLE (2.27 ± 2.05 ´ 104 and 4.14 ± 4.06 ´ 104 TREC/µg DNA, respectively) compared to quiescent SLE (5.83 ± 7.41 ´ 104 and 11.24 ± 15.06 ´ 104 TREC/µg DNA; p = 0.03, p = 0.02, respectively). Patients with active SLE had lower TREC levels in CD4+ T cells than controls (2.27 ± 2.05 ´ 104 vs 5.64 ± 4.99 ´ 104 TREC/µg DNA; p = 0.03), but this difference did not reach statistical significance for CD8+ cells (4.14 ± 4.06 ´ 104 vs 8.77 ± 8.78 ´ 104 TREC/µg DNA; p = 0.1). Patients with quiescent SLE presented TREC levels similar to controls in CD4+ and CD8+ cells (p = 0.49, p = 0.3, respectively).

Conclusion. Our results reveal decreased TREC levels in the peripheral blood of patients with active but not in patients with quiescent SLE. These data suggest that TREC levels are affected by disease activity in SLE. (First Release July 15 2008; J Rheumatol 2008;35:1762-7)

Key Indexing Terms:

SYSTEMIC LUPUS ERYTHEMATOSUS
T LYMPHOCYTE
THYMUS
T CELL RECEPTOR EXCISION CIRCLE


From the Rheumatology Division and Infectious Diseases Division Universidade Federal de São Paulo; and the Clinical Immunology and Allergy Division, University of São Paulo, São Paulo, Brazil.

Supported by The State of São Paulo Research Foundation (FAPESP grant 04/14795-6) and partially by the Brazilian Society of Rheumatology Research Agency.

Q.F. Vieira, BSc; C. Kayser, MD, PhD, Rheumatology Division; E.G. Kallas, MD, PhD, Infectious Diseases Division and Clinical Immunology and Allergy Division; L.E.C. Andrade, MD, PhD, Rheumatology Division, Universidade Federal de São Paulo.

Address reprint requests to Dr. L.E.C. Andrade, Universidade Federal de São Paulo (UNIFESP), Rheumatology Division, Rua Botucatu 740, 3° andar, São Paulo, SP, 04023-062, Brazil. E-mail: luis@reumato.epm.br

Accepted for publication April 7, 2008.




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