Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by the presence of auto antibodies, joint inflammation and subsequent destruction of cartilage and bone. The disease affects multiple organs, including the joints, skin, heart, lungs and eyes. However, the primary target of the abnormal autoimmune response is the synovial joints.
RA involves all elements of the immune response. It is initiated by immune complexes (ICs) and complement, perpetuated by cytokines and affected by metalloproteinase’s.
The local production of IgG and rheumatoid factors (RF), which are auto antibodi
es directed against the Fc portion of IgG, along with the antibodies to anti-cyclic citrullinated peptide lead to complement activation, appear important in
destructive events associated with the synovitis.