4.7 Article

Serum levels of tumour necrosis factor family members a proliferation-inducing ligand (APRIL) and B lymphocyte stimulator (BLyS) are inversely correlated in systemic lupus erythematosus

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ANNALS OF THE RHEUMATIC DISEASES
卷 68, 期 6, 页码 997-1002

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B M J PUBLISHING GROUP
DOI: 10.1136/ard.2008.090928

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  1. CHU Montpellier [AOI, UF 7821]
  2. Fondation de France
  3. Fondation pour la Recherche Medicale and Association pour la Recherche sur le Cancer
  4. Spanish National Research Council (CSIC)
  5. Pfizer

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Objective: To determine whether serum levels of a proliferation-inducing ligand (APRIL) are altered in patients with systemic lupus erythematosus (SLE), and correlate with disease parameters. Methods: Clinical and biological parameters were analysed for 43 patients that fulfilled American College of Rheumatology (ACR) criteria for SLE classification and were positive for anti-double-stranded DNA (dsDNA) antibodies at least once in their medical records. Tests included measurement of serum levels of the tumour necrosis factor (TNF) family members APRIL and B lymphocyte stimulator (BLyS; a cytokine shown to promote SLE disease). Results: Median APRIL levels were elevated in patients with SLE compared to patients with osteoarthritis and healthy controls, but did not correlate with the SLE Disease Activity Index (SLEDAI). APRIL serum levels showed an inverse correlation with BLyS serum levels (r = -0.339; p = 0.03). For patients with SLE with positive anti-dsDNA titres (>40 arbitrary units (AU)/ml) at inclusion (n = 25), circulating APRIL was inversely correlated with BLyS levels (r = -0.465; p = 0.022) and anti-dsDNA antibody titres (r = -0.411; p = 0.046). In a follow-up study at their second visit, 27 patients showed an inverse correlation of APRIL serum levels with BLyS (r = -0.398; p = 0.03) as well as with anti-dsDNA (r = -0.408; p = 0.03) titres and SLEDAI (r = -0.408; p = 0.01). Conclusion: The inverse correlation observed between APRIL and BLyS suggests that APRIL acts as a protective factor. APRIL and BLyS may thus have opposite roles in SLE, which must be considered when defining therapeutic applications of these cytokines.

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