Found in patients with SLE and the anti-synthetase syndrome (a subset of AIM), interstitial lung disease, polyarthritis, Raynaud’s phenomenon, and mechanic’s hands; these features may occur in various combinations or as an isolated manifestation, especially interstitial lung disease.

If SLE is clinically suspected, follow-up tests for antibodies to ribosomal P phosphoproteins (P0, P1, P2, C22 RibP peptide) are recommended; these antigens may be included in the routine ENA profile.

Anti-RibP antibodies have been associated in some studies with neuropsychiatric lupus, and in childhood-onset SLE with autoimmune hemolytic anemia.

If AIM, in particular the anti-synthetase syndrome, is suspected, it is recommended to perform follow-up tests for antibodies to tRNA synthetases; antigens are included in disease specific immunoassays (ie, inflammatory myopathy profile).

If AIM, in particular necrotizing myopathy, is suspected, it is recommended to perform follow-up tests for anti-SRP antibodies; the antigen is included in disease specific immunoassays (ie, inflammatory myopathy profile).

The fine distinction between AC-19 and -20 may depend on HEp-2 substrates and/or antibody concentration; antibodies to both RibP as well as tRNA synthetases may be undetected in HEp-2 IIFA-screening.

Anti-RibP antibodies have been reported in 10% of AIH patients without clinical or laboratory evidence of SLE

The prevalence of anti-RibP antibodies in SLE has been reported to range between 8 – 35% in a multicenter study

Less than 60% of the sera positive for anti-RibP antibodies have the AC-19 pattern at serum screening dilutions of 1/80 or higher; the coexistence of a weak nucleolar staining is relatively common

Less than 50% of sera having anti-tRNA synthetase antibodies have an AC-19 pattern at serum screening dilutions of 1/80 or higher

Most reports describing clinical association of anti-RibP antibodies do not actually show correlations with the AC-19 pattern as such.