| Literature DB >> 12215644 |
David M Lee1, Daniel S Friend, Michael F Gurish, Christophe Benoist, Diane Mathis, Michael B Brenner.
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.Entities:
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Year: 2002 PMID: 12215644 DOI: 10.1126/science.1073176
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728