title: [Abatacept].
abstract: Rheumatoid arthritis (RA) is an autoimmune disease that targets synovial joints and leads to bone destruction and joint deformity. T cell activations were shown to be involved in the onset of RA. T cells may control downstream inflammatory mediators reaching the synovium, where inflammation leads to joint destruction. However the treatment of RA has improved considerably in recent years through the introduction of DMARDs such as MTX, and anti-tumor necrosis factor therapy, there is still unmet medical need. Not a few patients experience an inadequate response to these therapies. Abatacept, a fusion protein of the extracellular domain of CTLA4 (a molecule inhibits the costimulatory pathway in T cell activation) and the Fc domain of human IgG1, was developed for the treatment of RA. Abatacept has shown long-term efficacy and safety in RA patients who were inadequate to MTX and/or anti-tumor necrosis factor therapy.
authors: Matsubara Mayflower Hospital.
authors: Takeshi
authors: T
authors: Nakamura
authors: Tsukasa
authors: T
authors: Matsubara
mesh_terms: D000069594:Abatacept; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology; D006801:Humans; D018796:Immunoconjugates / Q000627:therapeutic use*; D007249:Inflammation / Q000188:drug therapy / Q000276:immunology; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D016896:Treatment Outcome
chemical_list: D018501:Antirheumatic Agents; D018796:Immunoconjugates; D000069594:Abatacept