Nowadays, the name anti-RA33 defines autoantibodies that are directed to hnRNP-A2 and its splice variant hnRNP-B1. Anti-RA33 occur in approximately 30-35% of patients with RA, in 20-25% of patients with systemic lupus erythematosus and in 35-40% of patients with mixed connective tissue disease, being rare or absent in other arthritic conditions with a non-autoimmune etiology. Anti-RA33 can be easily detected by immunoblotting employing crude nuclear extracts or the recombinant antigen. Fo routine diagnostics also ELISA can be employed which is somewhat less sensitive than immunoblotting. The use of indirect immunofluorescence is of limited usefulness for detecting anti-RA33. The pathogenic role of anti-RA33 is not fully understood. Anti-RA33 and T cells directed against RA33, that can be found in about 60% of RA patients might contribute to autoimmune inflammation by immune complex formation or by virtue of secretion of cytokines that may initiate and drive the pathogenic process.