Abstract:
:Using rheumatoid arthritis (RA) and periodontitis mouse models, we demonstrate that RA and periodontitis share many pathological features, such as deregulated cytokine production, increased immune-cell infiltration, increased expression of Toll-like receptors (TLRs), and enhanced osteoclast activity and bone erosion. We reveal that genetic deletion of cathepsin K (Ctsk) caused a radical reduction in inflammation and bone erosion within RA joint capsules and periodontal lesions, a drastic decrease in immune-cell infiltration, and a significant reduction in osteoclasts, macrophages, dendritic and T-cells. Deficiency of Ctsk greatly decreased the expression of TLR-4, 5, and 9 and their downstream cytokines in periodontal gingival epithelial lesions and synovial RA lesions. Hence, Ctsk may be targeted to treat RA and periodontitis simultaneously due to its shared osteoimmune role.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Hao L,Zhu G,Lu Y,Wang M,Jules J,Zhou X,Chen Wdoi
10.1016/j.febslet.2015.04.008subject
Has Abstractpub_date
2015-05-22 00:00:00pages
1331-1339issue
12eissn
0014-5793issn
1873-3468journal_volume
589pub_type
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