11 September 2014
Researchers at the University of Illinois at Chicago (UIC) College of Medicine have shown that stopping a single receptor from being activated could prevent inflammation and bone degradation in rheumatoid arthritis.
The study, published in the Journal of Immunology, found that the activation of TLR5 - a receptor found on marrow-derived cells - is all that is needed to trigger cell migration to the fluid of arthritic joints.
Rheumatoid arthritis - a progressive autoimmune inflammatory disease of the joints - characterised by swelling and pain - is caused by cells migrating to the joints, which triggers progressive bone loss.
Dr Shiva Shahrara, UIC associate professor of rheumatology and corresponding author on the paper, and her team discovered the receptor is much more abundant on marrow-derived cells found in the fluid of joints in patients with rheumatoid arthritis, compared to samples from healthy subjects.
Previous research from the team had found that activating TLR5 caused abnormal blood vessel formation in rheumatoid arthritis patients. However, the new study determined it also controls an inflammatory molecule - TNF-alpha. This encourages more marrow-derived or myeloid cells into the joint, where they become bone-degrading cells - osteoclasts.
The researchers found that blocking the activation of TLR5 with an antibody significantly reduced the number of cells flooding to the joints.
Posted by Philip Briggs
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