1 Introduction
Systemic lupus erythaematosus (SLE) is a multisystem autoimmune disease characterized by the production of a large number of autoantibodies and a multitude of immune complex deposits in the target tissues. Antinuclear antibodies (ANAs) are a type of specific autoantibody that has been evaluated in clinical work to diagnose of systemic autoimmune rheumatic diseases (SARDs) and SLE since the 1940s[1,2]. Anti-double-stranded DNA (dsDNA) autoantibodies are important laboratory biomarkers related to disease activity in SLE[3]. The combined detection of ANAs and anti-dsDNA could improve the diagnostic specificity, sensitivity and disease activity of SLE, which compensates for the titre of ANAs that remain constant for a certain period of time. Although anti-dsDNA antibodies reveal high SLE specificity, their prevalence in different studies has been found to be only in 50% of SLE patients and does not always correlate with disease activity[4,5]. Likewise, we found that approximately 27.8% (27/97) of SLE patients were anti-dsDNA-negative, although patients’ clinical symptoms were active in our study.
Previous studies have shown that the B-cell-attracting chemokine CXC ligand 13 (CXCL13) is closely related to autoimmune diseases, especially SLE, rheumatoid arthritis (RA), Sjögren's syndrome and other autoimmune diseases[6,7,8,9,10]. CXCL13 is significantly increased in SLE patients, especially in lupus nephritis (LN) patients and is positively correlated with the SLE disease activity index (SLEDAI) and anti-dsDNA titre. The diagnostic sensitivity and specificity of LN are up to 95% and 88%, respectively[9]. However, the involvement of CXCL13 in SLE patients who are anti-dsDNA-negative still needs to be investigated further. Here, we assessed the regulatory response of CXCL13 in the serum of SLE anti-dsDNA-positive patients, SLE anti-dsDNA-negative patients, non-SLE patients and healthy controls. The changes in CXCL13 in the SLE patients after treatment were studied to evaluate the effects of CXCL13. In addition, the correlations between CXCL13 and clinical disease activities and laboratory results were studied to examine the possible mechanisms of CXCL13.