Context
The observations that IL-6 deficient mice are resistant to rheumatoid arthritis (RA) and anti-IL-6 receptor antibodies are an effective treatment for RA, have led to the conclusion that IL-6 is important in the development of disease. JAK tyrosine kinases and the STAT3 transcription factor are preferentially activated by IL-6, and STAT3 activation has been observed in RA synovium. CIS3 was recently identified as a negative regulator of the proinflammatory response and has been shown to inhibit STAT3 activation. Therefore, the authors have investigated the therapeutic potential of adenovirus-delivered dominant negative (dn) STAT3 and CIS3 in both antigen- and collagen-induced models of arthritis (AIA and CIA).