Chemokine ligand 13 (CXCL13) is believed to play a role in the recruitment of B cells in the central nervous system during neuroinflammation. Neurosyphilis is a group of clinical syndromes of the central nervous system caused by Treponema pallidum (T. pallidum) infection. The relationship between CXCL13 and neurosyphilis still needs further study. In our study, CSF and serum CXCL13 concentrations were detected among 40 neurosyphilis patients, 31 syphilis/non-neurosyphilis patients, 26 non-syphilis/other central nervous system diseases patients. Serum CXCL13 concentrations were detected in 49 healthy persons. All enrolled persons were HIV-negative. Receiver operating characteristic (ROC) analysis was performed to determine the threshold value that could distinguish neurosyphilis from syphilis. We found that the CSF CXCL13 concentrations and CXCL13 quotient (QCXCL13) were significantly increased in neurosyphilis patients compared to syphilis/non-neurosyphilis (χ2 = 21.802, P < 0.001) and non-syphilis patients (χ2 = 7.677, P = 0.002). ROC curve analyses revealed that CSF CXCL13 concentrations and QCXCL13 could serve as valuable biomarkers for differentiating neurosyphilis from non-neurosyphilis/syphilis. The CSF CXCL13 and QCXCL13 could serve as valuable biomarkers for differentiating neurosyphilis from non-neurosyphilis/syphilis in HIV-negative patients.

Objectives: The chemokine CXCL1, known as growth-related oncogene α (GRO-α), is a potent chemoattractant and regulator of neutrophils. The purpose of our study was to evaluate the regulatory response of CXCL1 in the serum of patients with systemic lupus erythematosus (SLE) in the active stage of disease and to assess whether it was implicated in the pathogenesis/inflammatory process in lupus. Methods: CXCL1 serum concentrations were examined in 90 SLE patients, 56 other autoimmune diseases (OADs) patients and 100 healthy controls using enzyme-linked immunosorbent methodology. Results: SLE patients exhibited significant increases in serum CXCL1 concentrations [1492.86 (735.47–2887.34) pg/ml] compared with OADs patients [155.88 (10.77–366.78) pg/ml] and healthy controls [13.58 (8.46–37.22) pg/ml] (p < 0.001). Moreover, the level of CXCL1 decreased as the level of anti-dsDNA IgG decreased after treatment between the anti-dsDNA-positive SLE patients and the anti-dsDNA-negative SLE patients. Additionly, serum CXCL1 concentrations were related to different disease activity levels in SLE and lupus nephritis (LN) and high avidity of IgG ANAs (HA IgG ANAs) (p < 0.05). Furthermore, CXCL1 serum concentrations were significantly correlated with the SLE Disease Activity Index(SLEDAI) score, relative avidity index (RAI) of HA IgG ANAs and the levels of anti-dsDNA IgG, CRP, ESR, albumin, C3 and C4.Additionally, Statistical analysis revealed that positivity for IgG ANA (p < 0.001), the presence of HA IgG ANAs (p = 0.001) and the logarithmic level of anti-dsDNA IgG (p = 0.021) were significantly associated with the logarithmic level of CXCL1 with standard partial regression coefficients (95% CI) of 2.371 (1.734–3.009), 1.231 (0.52–1.937) and 0.409 (0.062–0.755), respectively. Finally, using cutoff points of 1182.17 pg/mL and 1500.31 pg/mL, serum CXCL1 levels had a similar sensitivity of 76% and specificity of 100% and 75% for the diagnosis of active SLE and LN, respectively. Conclusions: Serum CXCL13 concentrations might represent a potential marker of disease activity in systemic lupus erythematosus.

Objectives: Our study purpose was to detect the distribution of anti-nuclear antibody (ANA) IgG subclasses in patients with systemic lupus erythematosus (SLE) and to evaluate their influence on the inflammatory process in SLE. Methods: We determined the serum levels of ANA IgG subclasses from 70 SLE patients, 25 patients with other autoimmune diseases (OAD), and 25 healthy controls using ELISA. The serum level of total ANA IgG and the avidity of ANA IgG, dsDNA IgG, and dsDNA IgG subclasses were analysed by ELISA. Results: The results indicated that levels of four ANA IgG subclasses (IgG1, IgG2, IgG3 and IgG4) and total IgG were significantly higher in SLE patients than in OAD patients and healthy controls ( p < 0.001). Moreover, the level of each ANA IgG subclass and the prevalence of high-avidity IgG ANAs (HA IgG ANAs) were significantly higher in the active cases than in the inactive cases of SLE and LN. Furthermore, level of ANA IgG subclasses decreased as level of dsDNA IgG subclasses decreased in 30 patients with SLE. In comparison, ANA IgG3 was significantly effective in high-dose prednisone combined with hydroxychloroquine ( p = 0.025). Additionally, it revealed that level of dsDNA IgG had a significant influence on four ANA IgG subclasses, especially on ANA IgG3 (β coefficient = 0.649, p < 0.001). Level of ANA IgG3 was also positively related to the serum level of dsDNA IgG (r = 0.729, p < 0.001 ) and RAI of HA IgG ANAs (r = 0.504, p < 0.001 ). However, the level of ANA IgG4 was positively related to the serum level of albumin (r = 0.572, p < 0.001 ) and RAI of HA IgG ANAs (r = 0.549, p < 0.001 ). Moreover, the results revealed that cutaneous and renal involvement were mainly associated with the ANA IgG1 and IgG4 subclasses. Although, arthritic involvement was mainly associated with ANA IgG3. Conclusions: First, we demonstrated that the ANA IgG subclasses were diagnostic tools in SLE patients. Furthermore, HA IgG ANAs might affect the distribution of ANA IgG3 and IgG4. Moreover, ANA IgG3 might play a particular role in the activity of SLE disease and therapy. Therefore, an altered ANA IgG subclass distribution might be a risk factor influencing the inflammatory process in SLE.