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Rheumatoid arthritis (RA) is characterized by inflammation and synovial proliferation. Drugs that target proinflammatory cytokines such as tumor necrosis factor (TNF)-α have advanced the treatment of RA, but because they do not always work, other treatments are required. A team from Harvard Medical School reports that an adhesion molecule on the surface of synovial cells, cadherin-11, triggers inflammation and synovial proliferation.
The team treated mice suffering from an RA-like disease with specific antibodies against cadherin-11, and with another drug that impairs the function of cadherin-11. Both treatments led to dramatically reduced destruction of cartilage and (to a lesser degree) bone. No adverse effects were noted.