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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

B细胞激活因子 医学 痹症科 内科学 免疫学 细胞因子 抗体 肿瘤坏死因子α 系统性红斑狼疮 结缔组织病 自身免疫性疾病 胃肠病学 疾病 B细胞
作者
Jérôme Morel,Camille Roubille,Lourdes Planelles,Clarissa Araújo Gurgel Rocha,Leticia Fernández,Cédric Lukas,M. Hahne,Bernard Combe
出处
期刊:Annals of the Rheumatic Diseases [BMJ]
卷期号:68 (6): 997-1002 被引量:76
标识
DOI:10.1136/ard.2008.090928
摘要

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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