Anti-ribosomal P protein antibodies

SARDs are a heterogeneous group of disorders characterized by dysregulation of the immune system, that starts to turn against the body’s own tissues. Major SARDs include systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis and Sjögren’s syndrome. These diseases can affect multiple organs and share common symptoms such as fatigue, fever, joint pain and skin rash. Diagnosis relies on a combination of clinical assessment and specific autoantibody tests. Early diagnosis is crucial to initiate appropriate therapy and slow down disease progression.

Anti-ribosomal P protein antibodies are directed against three phosphorylated proteins (P0, P1 and P2) of the 60S ribosomal subunit, which are involved in protein synthesis and GTPase activity. The immunodominant epitope is located in the common C-terminal region of the three phosphoproteins (peptide C22).

In indirect immunofluorescence on HEp-2 cells, these antibodies produce a fine, dense granular cytoplasmic pattern classified as AC-19. Anti-RibP antibodies are highly specific for systemic lupus erythematosus (SLE), with a prevalence ranging from 10% to 35%, and are rarely detected in other systemic autoimmune diseases. They may also be present in SLE patients who test negative for anti-dsDNA and anti-Sm antibodies.

Clinically, anti-RibP positivity has been associated with neuropsychiatric manifestations (particularly psychosis), childhood-onset SLE and autoimmune haemolytic anaemia. Associations have also been reported with lupus hepatitis and, in some studies, with increased disease activity.

Antibodies against ribosomal proteins may also be found in patients with Chagas disease and hepatitis C virus infection, although in these cases the recognised epitopes differ from those typical of SLE, suggesting molecular mimicry.