RHEUMATOID ARTHRITIS: ETIOPATHOGENESIS AND MOLECULAR BASIS

Abstract

Rheumatoid arthritis (RA) is the most common form of inammatory 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.