Summary
PROJECT SUMMARY Tumor necrosis factor (TNF)-α is a major inflammatory cytokine involved in the pathogenesis of several autoimmune and inflammatory diseases, including rheumatoid arthritis (RA). Current approaches aim to curb TNF-α-induced inflammation and tissue damage by treating patients with TNF-α inhibitors (specific antibodies or soluble receptors). The ineffectiveness of TNF inhibitors in >40% of patients partly indicates that we do not yet fully understand the underlying signaling mechanisms to effectively target TNF-α. While the use of TNF inhibitors has provided new insights into huma
