Cambridge, MA (August 15, 2006) – Researchers at Biogen Idec (NASDAQ: BIIB), a global biotechnology leader with products and capabilities in oncology, neurology and immunology, reported in the August 15, 2006 issue of the Journal of Immunology that activation of a recently discovered inflammation pathway may play an important role in the disease process that causes rheumatoid arthritis (RA). The studies advance the understanding of RA and demonstrate that inhibiting the TWEAK molecule may provide a new approach to developing RA treatments.
Discovered by Biogen Idec and University of Geneva scientists, TWEAK belongs to a family of molecules called tumor necrosis factor (TNF) that plays an important role in normal immune system and inflammatory responses. TNF-inhibiting therapies are currently used to treat a number of diseases including RA, a chronic, autoimmune disease that causes inflammation and swelling of the joints and the surrounding synovial tissue, resulting in progressive damage to the cartilage and bone.
TWEAK stimulates blood vessel growth (angiogenesis) and production of inflammatory proteins called cytokines and chemokines. The published studies found that TWEAK promotes a number of events that are hallmarks of rheumatoid arthritis, including joint inflammation and synovial angiogenesis (blood vessel growth in joints).
“Despite considerable progress, many rheumatoid arthritis patients do not adequately respond to current treatments, indicating that other pathways are involved in this complex disease,” said Timothy Zheng, Ph.D., Senior Scientist, Molecular Discovery at Biogen Idec. “Our investigative research suggests that TWEAK contributes to the disease through multiple mechanisms, and inhibiting the TWEAK pathway may represent a new set of opportunities for treatment.”
Specifically, the Biogen Idec researchers found that TWEAK promotes joint inflammation by stimulating the production of several types of inflammatory proteins, triggers joint damage by stimulating the production of damaging metalloprotease enzymes and promoting bone breakdown, and contributes to joint tissue disease by directly promoting angiogenesis in synovial tissue. The studies also suggest that TWEAK may impede normal bone repair mechanisms.
“Our research is part of a broader effort to identify the role of the TWEAK pathway in several autoimmune diseases,” added Linda Burkly, Ph.D., the TWEAK program leader at Biogen Idec.
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