Abstract
ObjectivesTo determine the presence and clinical associations of the soluble receptors of B cell‐activating factor from the tumor necrosis factor family (BAFF) in serum of patients with systemic lupus erythematosus (SLE).MethodsSerum BAFF and soluble BAFF receptor (sBAFF‐R) were quantified using ELISA, and soluble B cell maturation antigen (sBCMA) and transmembrane activator and cyclophilin ligand interactor (sTACI) by Luminex, in 87 SLE patients and 17 healthy controls (HC). Disease activity and organ damage were assessed using SLE Disease Activity Index 2000 (SLEDAI‐2K) and Systemic Lupus International Collaborating Clinics (SLICC) SLE Damage Index (SDI), respectively.Results BAFF and all receptors were detectable in all serum samples. Serum sBCMA and sTACI, but not sBAFF‐R, were significantly higher in SLE than in HC. Serum BAFF was also increased in SLE, but this association was attenuated after adjusting for age and ethnicity. Increased serum BAFF was associated with flare and organ damage. Increased serum sBCMA was associated with the presence of anti‐dsDNA, but not with overall or organ‐specific disease activity, flare or organ damage. Neither sTACI nor sBAFF‐R was associated with any SLE clinical parameters in multivariable analysis. While serum BAFF correlated negatively with sBAFF‐R in HC, no statistically significant correlations were observed between BAFF and its receptors in SLE patients.ConclusionSerum BAFF was associated with flare and organ damage independent of the presence of its soluble receptors. While sBCMA was associated with anti‐dsDNA positivity, other soluble BAFF receptors were not associated with SLE clinical indicators.
Highlights
Systemic lupus erythematosus (SLE) is an unpredictable and multifaceted chronic systemic autoimmune disease.[1]
One of the most prominent breakthroughs in SLE has been the discovery of the pathogenic role of B cell-activating factor from the tumor necrosis factor (TNF) family (BAFF) [ known as B lymphocyte stimulator (BLyS)]
BAFF-transgenic mice develop SLE-like features,[3] and high serum BAFF levels are a feature of some mouse models of SLElike disease.[4]
Summary
Systemic lupus erythematosus (SLE) is an unpredictable and multifaceted chronic systemic autoimmune disease.[1]. BAFF has a crucial role in B cell maturation, differentiation and survival, and is part of the BAFF/a proliferation-inducing ligand (APRIL) system. BAFF and APRIL ligate two cognate receptors, transmembrane activator and cyclophilin ligand interactor (TACI) and B cell maturation antigen (BCMA), and BAFF ligates BAFF receptor (BAFF-R).[2] These receptors transduce distinct signals; BCMA activation is important for long-lived plasma cell survival, BAFF-R activation for survival and maturation of immature B cells and TACI for B cell regulation, class-switch recombination and T cell-independent antibody responses.[2] BAFF-transgenic mice develop SLE-like features,[3] and high serum BAFF levels are a feature of some mouse models of SLElike disease.[4]
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