Rheumatoid arthritis is a chronic systemic inflammatory disease with major articular manifestations. While its aetiology still remains to be resolved, our understanding on the pathogenesis of rheumatoid arthritis has become clearer during two decades enlightening the role of adaptative immunity in the development of the symptoms and signs as well as in the progression of the pathological articular changes taking place in inadequately controlled disease. T lymphocytes are considered to be an important cell type in the pathogenesis of rheumatoid arthritis through production of proinflammatory cytokines, promotion of formation of ectopic lymphoid structures and neovascularization in synovial tissue, promotion autoantibody production by B cells, and activation of synoviocytes and osteoclasts. Abatacept, a CTLA4-Ig fusion protein, represents a new therapeutic approach in rheumatoid arthritis. Abatacept attenuates T cell activation as it regulates the activation of T cells by inhibiting the CD80/86:CD28 co-stimulatory pathway that is required for the proper T cell activation. This MiniReview gives an overview on the mechanism of action of abatacept and summarizes the published clinical data on abatacept in the treatment of rheumatoid arthritis.