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Cathepsin K-Dependent Toll-Like Receptor 9 Signaling Revealed in Experimental Arthritis
The scientists showed in their study that inhibition of cathepsin K effectively suppressed autoimmune inflammation of the joints as well as osteoclastic bone resorption in autoimmune arthritis. Cathepsin K-/- mice proved to be resistant against experimental autoimmune encephalomyelitis. Pharmacological inhibition or targeted disruption of cathepsin K led to defective Toll-like receptor 9 signalling in dendritic cells in response to unmethylated CpG DNA. In turn, T helper 17 cells activation was diminished, but the antigen-presenting ability of the dendritic cells was not affected.
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