A study supported by a grant from the National Institutes of Health and the Arthritis Foundation has linked the blood clotting protein fibrin with the development of rheumatoid arthritis (RA).

Fibrin deposits are a major feature of arthritic joints. It forms mesh-like matrices to create blood clots and these matrices may control local activity of inflammatory cells and support inappropriate tissue formation.

The research team at Cincinnati Children’s Hospital led by Dr. Jay Degen determined that inflammatory joint disease, such as RA, can result from the interaction between fibrin and a specific integrin receptor (aMB2) of inflammatory cells. An integrin receptor is a protein on a cell membrane that contributes to the function of the cell, such as a physiological response.

Dr. Degen stated that the findings suggest that therapies could be developed that would interrupt the interaction of fibrin and aMB2. These therapies might be effective for the treatment of RA as well as many other inflammatory diseases, such as multiple sclerosis.

The study, published in the November issue of The Journal of Clinical Investigation, was conducted using genetically engineered mice with collagen-induced arthritis of the knee and paw.