Fig. 3

IL-23 is required for the onset of GM-CSF- and TNF-driven arthritic pain and disease development. mBSA/GM-CSF (mBSA intra-articular (i.a.) [day 0]; GM-CSF or saline subcutaneous (s.c.) [day 0–2]) and mBSA/TNF (mBSA i.a. [day 0]; TNF or saline s.c. [day 0–2]) arthritis were induced in WT mice. The mice were treated i.p. with anti-IL-23p19 mAb or IgG1 isotype control, either a, b prophylactically (150 μg, days − 2 and 0) or c, d therapeutically (150 μg, on day 4 or day 1) for mBSA/GM-CSF and mBSA/TNF, respectively. Pain (incapacitance meter) and arthritis (histology, day 7) were assessed. Data are expressed as mean ± SEM; a, c WT mBSA/GM-CSF male mice (IgG1 isotype control, n = 5; anti-IL-23p19 mAb, n = 5), b, d WT mBSA/TNF male mice (IgG1 isotype control, n = 5; anti-IL-23p19 mAb, n = 5). For statistical analysis, a two-way ANOVA was used. *P < 0.05, **P < 0.01, ***P < 0.001, isotype vs. anti-IL-23p19 mAb