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.
复制标题
DOI:
10.1007/s00011-011-0324-7
复制
发表时间:
2011-07
影响因子:
6.7
通讯作者:
Davey, Michael P.
中科院分区:
文献类型:
--
作者:
Rosenzweig, Holly L.;Clowers, Jenna S.;Nunez, Gabriel;Rosenbaum, James T.;Davey, Michael P.
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.
登录
查看更多内容
DOI:
10.1084/jem.20021890
发表时间:
2003-05-05
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Brown GD;Herre J;Williams DL;Willment JA;Marshall AS;Gordon S
通讯作者:
Gordon S
影响因子:
6
作者:
de Hooge, ASK;van de Loo, FAJ;van den Berg, WB
通讯作者:
van den Berg, WB
影响因子:
56.9
作者:
DICARLO, FJ;FIORE, JV
通讯作者:
FIORE, JV
影响因子:
64.8
作者:
Gross, Olaf;Gewies, Andreas;Ruland, Juergen
通讯作者:
Ruland, Juergen
影响因子:
4.8
作者:
Girardin, SE;Travassos, LH;Mengin-Lecreulx, D
通讯作者:
Mengin-Lecreulx, D