Clinical and Diagnostic Value of Ribosomal p2 Autoantibodies in Systemic Lupus Erythematosus

Overview

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by production of autoantibodies directed against nuclear and cytoplasmic antigens. Clinically, this disorder is characterized by periods of remission and relapse (1). The early and accurate diagnosis of SLE is challenging (2). The SLE pathogenesis involves multiple cellular components of the innate and immune systems, presence of autoantibodies and immune complexes, engagement of the complement system and cytokine dysregulation (3). About 180 autoantibodies have been identified in SLE patients, 102 of which are reported to have an organ-specific correlation with SLE disease identified in SLE patients, with SLE disease activity (4). However, with the exception of autoantibodies such as antinuclear antibody (ANA), anti double stranded DNA (dsDNA), anti-smith and antiphospholipid antibodies, currently proposed by the American college of rheumatology (ACR) (5)

systemic lupus international collaborating clinics (SLICC) (6) for the diagnosis of SLE, most of these autoantibodies lack sufficient sensitivity and/or specificity for use in clinical diagnosis. Discovery of additional autoantibodies with high sensitivity and specificity is important for early diagnosis and assessment of the prognosis of SLE (7). Anti-ribosomal P(Anti-Rib-P) antibody, routinely tested in SLE, targets a homologous 22-amino acid C-terminal (C-22) sequence shared by three ribosomal phosphoproteins known as P0, P1, and P2 (8). The prevalence of anti-Rib-P antibody is about 15-40% in SLE patients and varies with the ethnicity, disease activity and detection method (9). Studies have disclosed that anti-P antibodies react with activated T cells but not with B cells, suggesting possible direct effects of anti-P antibodies on immune regulation (10).

Conditions