According to several reports IL-10 seems to play a pivotal role in the pathogenesis of SLE, although its exact function in vivo is not fully understood (Llorente et al. 2000). Among many immunomodulating activities, IL-10 is known to inhibit the production of several proinflammatory cytokines and to promote a Th2 immune response. Accordingly, IL-10 promotes B-cell differentiation and hyperactivity, but at high doses also seems to have an inhibitory effect on B-cell functions. Moreover, IL-10 upregulates Fas ligand-expression in vitro which may result in augmented T-cell death in vivo (Solsky and Wallace 2002). In mice IL-10 inhibits antigen presentation and Th1-lymphocyte activation (Yin et al. 2000). In patients with SLE an increased production of IL-10 by peripheral blood mononuclear cells was found to be associated with overproduction of pathogenic auto-antibodies. Therefore, it seemed reasonable to investigate whether blocking IL-10 may provide an useful approach to treat autoimmune diseases such as LE. Accordingly, six steroid-dependent patients with SLE were treated for 21 consecutive days with intravenous infusion of anti-IL-10 (20mg/d). Patients experienced a significant decrease in disease activity and were able to reduce concomitant steroid medication. In addition, a significant improvement of vasculitis and skin lesions was observed. Clinical scores remained stable through a follow-up of 6 months and no significant adverse events have been reported (Llorente et al. 2000).

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