par Baarsma, Goitze Seerp;Caspers, Laure 
Référence Intraocular Inflammation, Springer Berlin Heidelberg, page (331-338)
Publication Publié, 2016-01
Référence Intraocular Inflammation, Springer Berlin Heidelberg, page (331-338)
Publication Publié, 2016-01
Partie d'ouvrage collectif
| Résumé : | In 1976, Jean-Francois Borel et al. [1] described the possible use of cyclosporin A (CsA) for the treatment of autoimmune disease. Since then, CsA has been studied in virtually every known autoimmune disease in man, ranging from systemic lupus erythematosus (SLE), psoriasis and inflammatory bowel disease to rheumatoid arthritis and to diseases like asthma. Although the pathogenesis of endogenous uveitis, especially endogenous posterior uveitis (EPU), is still incompletely understood, it has become clear that the disease is a T-cell-mediated disease. Before the introduction of CsA, the mainstay of therapy was corticosteroids, sometimes used in combination with azathioprine, methotrexate, or cytotoxic agents such as cyclophosphamide and chlorambucil. However, these therapies frequently failed to control EPU adequately and need to be high dosed, resulting in a high incidence of toxicity. The immunosuppressive actions of CsA are (relatively) specific for T lymphocytes. In these cells, CsA blocks several intracellular signalling processes, causing a decreased transcription of the IL-2, IL-4, CD40L and γ-interferon genes, which finally results in the inhibition of the activation and proliferation of T lymphocytes. |
