Are anti-ribosomal P protein antibodies relevant in systemic lupus erythematosus?

Systemic lupus erythematosus (SLE) is a prototypal auto-immune disorder characterized with multiple organ involvement resulting in disability and increased mortality. Immune regulatory disturbances cumulate in activation of B cells and consequent auto-antibody production. Antigens for these auto-antibodies can be nuclear components and cytoplasmic elements. Anti-P antibodies react against acidic phosphorylated ribosomal proteins P0, P1, and P2 (with molecular mass of 38, 19, and 17 kDa, respectively) and are located on the S60 subunit of ribosomes. Ribosomal P proteins share a common 22-amino acid sequence that is present in the carboxyl-terminal. Anti-P antibodies can be detected in approx 15 to 20% of patients with lupus by several immunoassays, most frequently by enzyme-linked immunosorbent assay (ELISA) and/or Western blotting. However, no standardized assay is available. Auto-antibodies against eukaryotic P proteins appear highly specific for SLE; therefore, they can be used as diagnostic marker for the disease. Furthermore, association has been described with particular manifestations of lupus, especially with neuropsychiatric, renal, and hepatic involvements. Anti-P positivity and the titer of anti-P antibodies also fluctuate with clinical disease activity. Despite several lines of evidence, results are conflicting regarding the existence of such associations. Discrepancies can be explained by different study set-up or study population; it also can be attributed to the different sensitivity of tests used for the detection of anti-P antibody.