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These CS-induced EVs had no obvious effect on the number and cytokine production (TNF, IL-6, IL-23) of dendritic cells, as well as the polarization of M0 macrophages, but they acted as a proinflammatory factor that induced osteoclastogenesis by inhibiting cyclooxygenase-2 (COX-2), revealing a mechanism of CS signaling and offering a potential target for therapeutic interference of inflammatory disease [99]
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