Thrombin cleavage site huTNFR-
Figure 6 Schematic diagram of TNF and IL-1 receptor fusion proteins utilized in arthritis gene therapy.
degradation. Moreover, the two vectors together appeared to have an additive effect on white blood cell infiltration into the joint space. There was also an effect observed on contralateral joints in this study . Le and colleagues also demonstrated efficacy of the TNF inhibitor gene in a rat model of CIA . Interestingly, Quattrocchi have reported in a mouse model of CIA that there is an acute beneficial effect of the TNF inhibitor fusion protein; however, there is a subsequent rebound with enhanced inflammation despite continued circulating levels of the TNF inhibitor. The investigators speculated that this may be due to antibody formation against the extracellular domain of the receptor that the cross-linked endogenous TNF receptors in the joint . It is important to note that these studies were performed with a chimeric fusion protein (mouse Fc/human p55 TNF receptor) and thus whether the exacerbation of arthritis would be seen with the mouse p55 TNF receptor remains to be seen. Last, Zhang and colleagues have shown that adenoviral-mediated gene transfer of a dominant negative form of inhibitory kappa-B, which facilitates nuclear translocation of nuclear factor-kappa-B, enhanced TNF-mediated apoptosis in synovial tissue .
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