Abstract
Connective tissue diseases are generated by different immunoregulatory alterations. Their better knowledge may lead to new treatment modalities. In systemic lupus erythematosus (SLE), increased IL-10 production by non-T cells might exert an inhibitory effect on Thl CD4+ T cells which would explain the decreased T cell functions observed in these patients. In rheumatoid arthritis (RA) patients, there may be a balance within the synovium, where the local production of IFN-gamma may limit the anti-inflammatory properties of IL- 10, thus leading to chronic damage. This article shows that rational approaches to therapy need to be individualized. In SLE, the potential therapeutic use of monoclonal antibodies to IL-10 seems to be gathering strength, whereas in RA exactly the opposite is contemplated: IL-10 is tried for its potential therapeutic use.
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