Rheumatoid Arthritis: A New Villain

By Sondra Forsyth

Researchers have discovered that one key receptor plays a big part in provoking rheumatoid arthritis.

The finding, by investigators from the University of Illinois at Chicago College of Medicine, means that there is now a new target for potential treatments of RA.

The receptor, TLR5 or toll-like receptor 5, begins the damaging process of inflammation and bone degradation that characterizes RA, the researchers said. It’s found on cells in the fluid of arthritic joints.

“TLR5 does it all,” said Shiva Shahrara, UIC associate professor of rheumatology and corresponding author on the paper. TLR5, or toll-like receptor 5, is found on myeloid, or marrow-derived, cells that migrate from the blood into affected joints.

Using a mouse model, Shahrara and her colleagues found that the receptor is much more abundant in mice with RA as compared with mice who don’t have the condition. They also discovered that the receptor works with an inflammatory molecule called TNF-alpha to aggravate RA.

Based on the mouse study, Shahara said she believes a drug that prevents TLR5 activation could slow or prevent the inflammation and bone erosion of later-stage rheumatoid arthritis in humans.

The findings were published in the Journal of Immunology.