Figure 1.

IL-17 induced expression of interleukin (IL)-32 via NF-κB and PI3 kinase in fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). (A) FLSs from RA patients (RA FLSs) were cultured with increasing doses (1 and 5 ng/ml) of IL-17 for 12 h. IL-32 mRNA levels were measured by real-time PCR. ***P < 0.001 (in comparison with nil), ** P < 0.01 (in comparison with nil). (B) RA FLSs were pretreated with the signal inhibitors parthenolide (10 μM) or LY294002 (10 μM) for 2 h and then cultured with IL-17 (10 ng/ml) for 12 h. The IL-32 mRNA level was measured by real-time PCR. *P < 0.05 (in comparison with IL-17), **P < 0.01 (in comparison with IL-17). A and B show the means ± SD of more than three separate experiments. (C) Expression of IL-17, IL-32, phospho-IkB (p-IkB), NF-κB (p50), NF-κB (p65), phospho-Akt (p-Akt) and AKT in the synovium of patients with RA or osteoarthritis (OA). Immunostaining was performed using specific antibodies. Data are representative of three experiments with similar results.

Moon et al. Arthritis Research & Therapy 2012 14:R246   doi:10.1186/ar4089
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