CINCINNATI, Nov. 16 (UPI) -- U.S. researchers say the discovery of a link between a blood clotting protein and rheumatoid arthritis could lead to new therapies for the disabling disease.

   Jay Degan, a researcher in Developmental Biology at Cincinnati Children's Hospital, said inflammatory joint disease appears to be driven by the engagement of inflammatory cells with fibrin matrices through a specific integrin receptor, aMB2.

   The report, published in The Journal of Clinical Investigation, suggests that therapies designed to interrupt the localized interaction of inflammatory cells and fibrin may help arthritis patients.

   "Our study establishes that fibrin is a powerful, although context-dependent, determinant of inflammatory joint disease," Degen, the study's lead author, said Friday in a release. "These findings also suggest that pharmacologically interrupting the interaction of fibrin and aMB2 might be efficacious in the treatment of arthritic disease as well as many other inflammatory diseases, such as multiple sclerosis."

   Degen said the mesh-like matrices formed by fibrin to create blood clots may control local activity of inflammatory cells as well as support inappropriate tissue reorganization.
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