text: Conclusions
  We have detected a more pronounced production of IL-17 from RA PBMC in response to IL-15 and MCP-1 as well as stimulation by anti-CD3/anti-CD28. We have also shown that upregulation of IL-17 by activated T cells in patients with RA could be the result of activation via the PI3K/Akt pathway with resultant NF-kappaB activation. Our data provide insights into cellular mechanisms of the regulation of IL-17 production in RA, and highlight the role of T cells, which has hitherto been neglected in RA pathogenesis. Together with recent data on the successful introduction of anti-IL-17 in RA, our results have added information for the future molecular targeting of new therapeutic applications in RA. 
  