Mast cells: A cellular link between autoantibodies and inflammatory arthritis
Mast cells: A cellular link between autoantibodies and inflammatory arthritis
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DOI：
10.1126/science.1073176
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发表时间：
2002-09-06
期刊：
影响因子：
56.9
通讯作者：
Brenner, MB
中科院分区：
文献类型：
--
作者：
Lee, DM;Friend, DS;Brenner, MB
先前的研究表明，自身抗体，补体成分和Fc受体各自参与K/BxN小鼠糜烂性关节炎的发病机制。然而，尚不清楚哪些细胞群体对这些炎症信号有反应。我们发现肥大细胞缺陷的两种小鼠品系W/W-v和Sl/Sl（d）对关节炎症的发展具有抵抗力，并且通过肥大细胞移植，W/W-v品系的易感性得到恢复。因此，肥大细胞可能在炎症性关节炎中作为自身抗体、可溶性介质和其他效应物群体之间的细胞联系。
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/W-v and Sl/Sl(d) were resistant to development of joint inflammation and that susceptibility was restored in the W/W-v 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.