text: Conclusion
  CD4+ T cells from active RA patients are characterized by their resistance to IL-10 inhibition of IFN-gamma production, due to constitutive STAT3 phosphorylation and impaired IL-10-mediated STAT3 activation. The defective STAT3 signaling is possibly associated with SOCS1 predominance over SOCS3. These abnormalities in active RA are thought to be induced mainly after chronic exposure to high concentrations of IL-6. The limited efficacy of IL-10 treatment of RA patients [50] may be explained in part by the unresponsiveness to IL-10 of inflammatory cells, including T cells. On the contrary, the therapeutic efficacy of anti-IL-6 receptor antibody has been reported in RA patients [51], and one of the effects of this therapy may be to normalize T cells through the inhibition of IL-6-dependent STAT3 activation. More specific therapy targeting STAT3 activation will be awaited; for example, the induction of the SOCS3 gene, the efficacy of which has been demonstrated in animal models [37]. 
  