Our results showed that local administration of recombinant IL-27 onto calvariae of mice significantly alleviated osteolytic lesions. IL-27 inhibited the differentiation of osteoclasts in vitro. These results agree with concept that IL-27 can inhibit both RANKL-dependent osteoclastogenesis pathways through inducing STAT1 expression that inhibits c-Fos and NFATcl. These transcription factors are indispensable for osteoclast differentiation . In experimental rheumatoid arthritis mouse models, administration of IL-27 at the onset of the disease results in a reduction in serum inflammatory cytokines and disease severity compared with controls. On the contrary, administration of IL-27 in later phase of disease results in an elevation in production of inflammatory cytokines and consequently severity of disease . Together, our data suggest that IL-27 is a potential new target for novel therapeutic agent for aseptic loosening. However, due to its dual role in inflammation, should be carefully investigated before clinical therapy application.
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