Inhibition of STAT3 or NF-κB signaling or both reverses the production of IL-23, IL-17, IL-6, TNF-α, and IL-1β stimulated by TLR2 ligation. The production of IL-23 (a), IL-17 (b), IL-6 (c), TNF-α (d), and IL-1β (e) induced by TLR2 ligand in the presence or absence of inhibitor of STAT3 or NF-κB or both. Peripheral blood mononuclear cells from patients with SS (n = 5) were cultured with TLR2 ligand (PGN) in the presence or absence of STAT3 inhibitor (AG490 4, 20, and 100 μM) or NF-κB inhibitor (parthenolide 10 μM) or both for 48 hours. The concentrations of IL-23, IL-17, IL-6, TNF-α, and IL-1β in the culture supernatants were measured by sandwich enzyme-linked immunosorbent assay. Data are expressed as the mean ± standard deviation. *P < 0.05, **P < 0.01 compared with PGN-treated cells. #P < 0.05, ##P < 0.01 compared with PGN- and NF-κB inhibitor-treated cells. IL, interleukin; NF-κB, nuclear factor-kappa-B; PGN, peptidoglycan; SS, Sjögren's syndrome; STAT, signal transducer and activator of transcription; TLR, Toll-like receptor; TNF-α, tumor necrosis factor-alpha.
Kwok et al. Arthritis Research & Therapy 2012 14:R64 doi:10.1186/ar3780