Rheumatoid arthritis is a chronic systemic autoimmune disease characterized by inflammation of the joints, extraarticular involvement and the production of autoantibodies. In the affected joints proliferation of the synovial membrane occurs as well as neovascularization and infiltration of different cell types. Clinically rheumatoid arthritis is manifested as a heterogeneous disease and therefore it is not easy to investigate its genetic background. The genetic basis of rheumatoid arthritis is very complex with a significant contribution of molecules of the main histocompatibility complex. The authors discuss the part played by these genetic factors as well as the polymorphism of genes for some cytokines, immunoglobulins and the T cell receptor in the pathogenesis of rheumatoid arthritis.

        Key words: rheumatoid arthritis, genetic predisposition, genes, polymorphism, HLA, TNF-al- pha, TCR, Ig