Researchers at the University of California, San Diego (UCSD) School of Medicine have discovered that blocking an intracellular signaling enzyme in a key pathway may lead to effective new treatments to fight rheumatoid arthritis.
This discovery is exciting because it could potentially lead to less expensive and, hopefully, safer drugs to treat rheumatoid arthritis, said Gary S. Firestein, M.D., Professor of Medicine, Chief of the Division of Rheumatology, Allergy and Immunology, and Director of UCSD’s Clinical Investigation Institute.
Patients with rheumatoid arthritis are commonly treated with a class of drugs that treat symptoms by blocking the action of a protein called tumor necrosis factor (TNF). TNF is a component of the body’s immune system that triggers inflammation during normal immune responses. When overproduced, TNF can lead to excessive inflammation such as that experienced by patients with rheumatoid arthritis. However, such treatments can suppress normal immune responses, must be administered by injection rather than taken orally, and are very expensive.
For many years, researchers have explored developing better therapeutic targets by blocking the function of a family of enzymes called p38 MAP kinase, which regulate cytokines – proetin secreted in response to stress that regulate inflammation – in patients with arthritis.