Mast Cells: A Cellular Link Between Autoantibodies and Inflammatory Arthritis

David M. Lee(Brigham and Women's Hospital), Daniel S. Friend(Brigham and Women's Hospital), Michael F. Gurish(Brigham and Women's Hospital), Christophe Benoıst(Joslin Diabetes Center), Diane Mathis(Joslin Diabetes Center), Michael B. Brenner(Brigham and Women's Hospital)
Science
September 5, 2002
Cited by 744

Abstract

Previous studies have revealed that autoantibodies, complement components, and Fc receptors each participate in the pathogenesis of erosive arthritis in K/BxN mice. However, it is not known which cellular populations are responsive to these inflammatory signals. We find that two strains of mice deficient in mast cells, W/Wv and Sl/Sld, were resistant to development of joint inflammation and that susceptibility was restored in the W/Wv strain by mast cell engraftment. Thus, mast cells may function as a cellular link between autoantibodies, soluble mediators, and other effector populations in inflammatory arthritis.


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