Objective: Anti-ribosomal P (anti-P) antibody is a serological specific marker of systemic lupus erythematosus (SLE). The aim of this study is to investigate the association of this antibody with clinical and serological disorders in SLE. Methods: All relevant literature was retrieved from PubMed, EMBASE, Web of Science and CNKI databases. The qualities of these studies were evaluated using a modified version of the Newcastle–Ottawa scale. The associations of anti-P antibody with clinical and serological disorders were determined by the pooled odds ratio (OR) and the confidence interval (CI) calculated using meta-analysis with the Mantel–Haenszel method. Results: Sixteen cohort studies with 2355 patients were included in this study. Malar rash, oral ulcer and photosensitivity were strongly associated with serum anti-P antibody, with OR (95% CI) values of 2.05 (1.42–2.92), 1.49 (1.05–2.13) and 1.44 (1.08–1.91), respectively. Arthritis and renal involvement were not associated with anti-P antibody, whereas a high heterogeneity was observed due to ethnicity and publication bias, respectively. Neuropsychiatric SLE (NPSLE), hepatic involvement, anti-dsDNA, anti-Sm and anti-cardiolipin antibodies (aCL) were observed more frequently in anti-P positive patients than in negative patients. Studies on hepatic involvement showed a low precision with substantially broad CI (2.56–11.2). A high heterogeneity presented among studies on NPSLE, anti-Sm and aCL. Conclusions: Anti-P antibody is significantly associated with malar rash, oral ulcer, photosensitivity and serum anti-dsDNA antibody, and potentially associated with NPSLE, hepatic damage, serum anti-Sm and aCL.

Objective: The specific autoantibodies and antigens that mediate systemic lupus erythematosus (SLE)–related organ injuries remain largely unknown. This study was undertaken to investigate the antibody‐mediated immune response that leads to SLE skin lesions.Methods: The study included 85 SLE patients with lupus‐specific skin lesions and 31 without skin lesions. The reactivity of serum antibody with skin antigens was determined by immunoblotting using human foreskin as the substrate. Skin antigens were identified using mass spectrometry. Serum antibody was isolated by affinity purification and was injected intracutaneously into mouse skin to determine pathogenicity. Serum antibody levels were monitored by enzyme‐linked immunosorbent assay.Results: We determined that 78% of the patients with skin lesions had serum antibodies reactive with 35‐kd and/or 25‐kd skin antigens, which was significantly higher than the percentage of patients without skin lesions (P < 0.0001), suggesting a correlation between immune response and skin lesions. Acidic ribosomal protein P0 (RPLP0) and galectin 3 were 2 target antigens identified from 35‐kd and 25‐kd proteins, respectively. Purified serum anti‐RPLP0 and anti–galectin 3 antibodies induced lupus‐like histologic changes after intracutaneous injection. Anti‐RPLP0 and anti–galectin 3 antibody levels were significantly higher in SLE patients than in healthy controls and decreased with skin recovery. Anti–galectin 3 antibody levels were not significantly higher in SLE patients than in patients with dermatomyositis or scleroderma, but strongly related to lupus cutaneous vasculitis. Additionally, levels of the 2 antibodies were positively correlated with leukopenia and C3 deficiency, and the anti‐RPLP0 antibody level was also positively correlated with arthritis and SLE disease activity.Conclusion: Our findings indicate that the immune response mediated by serum anti‐RPLP0 and anti–galectin 3 antibodies plays a key role in the pathogenesis of SLE skin lesions. These findings provide new insights into the mechanism of SLE‐related organ disorders.