Rheumatoid arthritis (RA) is a chronic inflammatory disease one characteristic of which is the deposition of the protein fibrin in the joints, where it forms a matrix that contributes to the loss of joint mobility and function.
In a new study, Jay Degen and colleagues from Cincinnati Children’s Hospital Research Foundation, Cincinnati, have shown that in mouse models of inflammatory joint disease fibrin and its precursor fibrinogen are factors that contribute to the development of disease.
Mice lacking fibrinogen or expressing a mutant form of fibrinogen that is unable to bind the integrin alpha-M-beta-2 developed less severe joint disease than normal mice when administered collagen (the collagen-induced arthritis model of RA). Inflammatory cells still accumulated in the joints, but these cells produced less of the proinflammatory cytokines TNF-alpha, IL-1-beta, and IL-6. Consistent with a role for fibrinogen and fibrin upstream of proinflammatory cytokine production, joint disease induced by overexpression of TNF-alpha was not attenuated in mice lacking fibrinogen. The authors therefore suggest that blocking the interaction between fibrinogen and alpha-M-beta-2 might provide a new approach to treating individuals with arthritic disease.
TITLE: Fibrin(ogen) exacerbates inflammatory joint disease through a mechanism linked to the integrin alpha-M-beta-2 binding motif
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Sub-editorRheumatoid Arthritis :: Interrupting interactions might benefit individuals who are arthritic
by Sub-editor ( Author at Spirit India )
Posted on October 13th, 2007 at 5:49 am.
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