IL-17 induces monocyte migration in rheumatoid arthritis.
IL-17 induces monocyte migration in rheumatoid arthritis.
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DOI：
10.4049/jimmunol.0802246
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发表时间：
2009-03-15
期刊：
影响因子：
--
通讯作者：
Pope RM
中科院分区：
文献类型：
--
作者：
Shahrara S;Pickens SR;Dorfleutner A;Pope RM
Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease which is in part mediated by the migration of monocytes from blood to RA synovial tissue, where they differentiate into macrophages and secrete inflammatory cytokines and chemokines. The T cell cytokine IL-17 is expressed in the RA synovial tissue and synovial fluid. In order to better understand the mechanism by which IL-17 might promote inflammation, its role in monocyte trafficking was examined. In vivo, IL-17 mediates monocyte migration into sponges implanted into severe combined immunodeficient (SCID) mice. In vitro, IL-17 was chemotactic, not chemokinetic, for monocytes at the concentrations detected in the RA synovial fluid. Further, IL-17-induced monocyte migration was mediated by ligation to IL-17 receptor (R) A and C expressed on monocytes and was mediated through p38MAPK signaling. Finally, neutralization of IL-17 in RA synovial fluid or its receptors on monocytes significantly reduced monocyte migration mediated by RA synovial fluid. These observations suggest that IL-17 may be important in recruiting monocytes into the joints of patients with RA, supporting IL-17 as a therapeutic target in RA.
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