Dectin-1 and NOD2 mediate cathepsin activation in zymosan-induced arthritis in mice.

Dectin-1 and NOD2 mediate cathepsin activation in zymosan-induced arthritis in mice.
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DOI:
10.1007/s00011-011-0324-7
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发表时间:
2011-07
影响因子:
6.7
通讯作者:
Davey, Michael P.
Davey, Michael P.
中科院分区:
医学2区
文献类型:
--
作者:
Rosenzweig, Holly L.;Clowers, Jenna S.;Nunez, Gabriel;Rosenbaum, James T.;Davey, Michael P.

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模式识别受体(PRR)的激活可能有助于关节炎。在这里,我们阐明了NOD 2的作用,炎症性关节炎的遗传原因,和其他几个PRR在炎症性关节炎的小鼠模型。CR 3,TLR 2,MyD 88,NOD 1,NOD 2,Dectin-1和Dectin-2的作用在关节内注射酵母多糖,真菌细胞壁成分凝胶多糖,海带多糖和甘露聚糖,和细菌细胞壁肽聚糖引起的关节炎中进行了体内测试。Dectin-1和Dectin-2在较小程度上导致关节炎。TLR 2、MyD 88和CR 3起非必需作用。基于注射凝胶多糖、海带多糖或甘露聚糖的观察结果支持Dectin-1途径在关节中的主导作用。我们证明了NOD 1和NOD 2的不同作用,并确定NOD 2作为酵母多糖诱导的关节炎的一种新的和必不可少的介质。Dectin-1和NOD 2是酵母聚糖致关节炎作用中的关键性哨兵受体。我们的数据确定了NOD 2在关节内炎症反应中的新作用。
Activation of pattern recognition receptors (PRR) may contribute to arthritis. Here, we elucidated the role of NOD2, a genetic cause of inflammatory arthritis, and several other PRR in a murine model of inflammatory arthritis. The roles of CR3, TLR2, MyD88, NOD1, NOD2, Dectin-1 and Dectin-2 were tested in vivo in arthritis elicited by intra-articular injections of zymosan, the fungal cell wall components curdlan, laminarin and mannan, and the bacterial cell wall peptidoglycan. Dectin-1, and to a lesser extent Dectin-2, contributed to arthritis. TLR2, MyD88 and CR3 played non-essential roles. Observations based on injection of curdlan, laminarin or mannan supported the dominant role of the Dectin-1 pathway in the joint. We demonstrated differential roles for NOD1 and NOD2 and identified NOD2 as a novel and essential mediator of zymosan-induced arthritis. Together, Dectin-1 and NOD2 are critical, sentinel receptors in the arthritogenic effects of zymosan. Our data identify a novel role for NOD2 during inflammatory responses within joints.
Dectin-1介导β-葡聚糖的生物学作用。
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