Clinical Information

Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease that affects multiple organ systems with diverse clinical presentations. The disease is characterized by a diversity of antinuclear antibody (ANA) specificities associated with positivity of nuclear and/or cytoplasmic patterns using the HEp-2 substrate by indirect immunofluorescence assay (IFA).(1,2) Of the ANA-specific autoantibodies, only anti-dsDNA and anti-Smith antibodies associated with the Hep-2 substrate IFA nuclear patterns are required in contemporary classification criteria for SLE.(3,4) Detection of non-criteria SLE autoantibodies and their associated  profiles are fundamental in the clinical management of patients as these antibodies provide important clues for diagnosis, phenotypic categorization, and disease activity, as well as potential therapeutic targets.(5) For example, these autoantibodies may be involved in the inflammatory and immune complex formation causing damage in multiple end-organs such as kidney, skin, and central nervous system (CNS).

Anti-ribosomal P protein (anti-Rib-P, anti-P) antibodies were initially described in the 1980s and subsequently reported to recognize three specific ribosomal proteins (P0, P1 and P2, of 38, 19 and 17 kDa molecular weight, respectively) located in the large ribosome's subunit.(6).  A 2015 systematic review and meta-analysis of published studies reported significant association with malar rash, oral ulcer, photosensitivity and anti-dsDNA antibody positivity.(7) However, the associations with neuropsychiatric SLE, hepatic damage, serum anti-Smith and anti-cardiolipin antibodies were observed more frequently in anti-Rib-P positive patients than in negative patients. In a more recent meta-analysis, significant associations were noted for CNS involvement and psychosis, and lupus hepatitis with heterogeneity between studies for lupus nephritis.(6)  In a recent large single center study, anti-Rib-P antibody positivity was associated with a higher proportion of neurological involvement (p <0.05) at baseline.(8) In the same study, antibody-positive patients for anti-Rib-P antibodies were more likely to accumulate neuropsychiatric damage (adjusted HR = 3.8, 95% CI 2.7-57), p <0.001). The variable clinical associations between positivity for anti-Rib-P antibodies and the reported SLE manifestations in these and other studies may be due to demographic and clinical heterogeneity of the cohorts and different formulations of the immunoassays and methods for detecting antibodies.(6,9)

Anti-ribosomal antibodies can be detected and quantified using a variety solid-phase immunoassays in the clinical laboratory. The use of different antigenic combinations and antigens from different sources limit commutability between testing methods.(6)