Rheumatoid arthritis (RA) is the most common form of inammatory arthropathy sustained by autoimmune responses.
This review has the objective of updating the knowledge about RA especially its molecular pathogenesis. We examine
here the current knowledge of tryptophan, arginine, homoarginine and histidine metabolism and the main immunoregulatory pathways in amino
acid catabolism in both RA patients and experimental models of arthritis. Of the characteristic autoantibodies of RA, those that appear earlier, are
those that recognize cyclic citrullinated peptides. (CCP) and/or citrullinated brinogen. Therefore our analysis would indicate that amino acids
metabolism represents a fruitful area of research for new drug targets for a more effective and safe therapy of RA.