Elevated serum soluble CD27 levels are associated with both disease activity and humoral immune activity in patients with rheumatoid arthritis

Abstract

Objective: To investigate the serum level of soluble CD27 (sCD27) and its potential clinical significance in rheumatoid arthritis (RA). Methods: The serum sCD27 levels in both RA and health controls (HCs) were detected by enzyme-linked immunosorbent assay. The medical information and laboratory data of the patients were collected. The serum sCD27 levels in RA with different clinical features were analyzed, and the correlation between the clinical data and serum sCD27 levels were also analyzed. Independent samples t test, Mann-Whitney U-test or Wilcoxon signed-rank test, Spearman correlation were used for statistical analysis. Results: The levels of sCD27 were elevated in the RA patients (5647 ± 6526 pg/mL) than those of HCs (1659 ± 648 pg/mL) (P < 0.001). In addition, serum sCD27 levels were correlated with age, erythrocyte sedimentation rate, C-reactive protein (CRP), rheumatoid factor (RF), immunoglobulin A, immunoglobulin G, Complement 4 and disease activity score in 28 joints in RA patients. The levels of sCD27 were higher in the RF-positive RA patients (6522 ± 7447 pg/mL) than the RF-negative patients (3902 ± 2098 pg/mL), and the similar finding was also observed in anti-cyclic citrullinated peptide (anti-CCP) antibody positive (6241 ± 7207 pg/mL) and anti-CCP negative RA patients (4183 ± 2187 pg/mL). The RA patients with increased sCD27 and increased CRP showed the highest ratio of osteoporosis complication (P < 0.001). Conclusion: Serum sCD27 might be a promising biomarker which could reflect both disease activity and humoral immunity activity in RA.

Histological Evaluation of Arthritis in Mice

“…In patients with arthritis, radiofrequency absorption can be seen as a sign of serious disease in which B cell activity is significantly impaired [56,57]. Recent clinical trials using B cell depletion ensure the idea that humoral immunity produced by RF could play a significant role development of RA [58][59][60]. Inhibition or stimulation of inflammatory mediators, pro-inflammatory cytokines and immune cells may be involved in RA pathogenesis [61,62].…”