Anti–IL-23 therapy inhibits multiple inflammatory pathways and ameliorates autoimmune encephalomyelitis
J. Clin. Invest. Yi Chen, et al. 116:1317 doi:10.1172/JCI25308 [Go to this article.]

Figure 4
T-bet and TIM3 expression in IFN-γ– and IL-17–producing T cells. (A) Lymph node cells from naive C57BL/6 WT mice and T-bet– or STAT1-deficient mice were stimulated with soluble anti-CD3 for 48 hours in the presence or absence of IL-23. IL-17 levels in the culture supernatant were measured by ELISA. Data are mean cytokine production ± SD of separate lymph node cultures from 3 mice and are representative of 3 independent experiments. (B) SJL mice were immunized with PLP_139–151, and DLN cells were cultured with 20 μg/ml PLP peptide either in Th1-promoting conditions (IL-12 with blocking anti–IL-17 and anti–IL-23p19) or Th17-promoting conditions (IL-23 with blocking anti–IFN-γ and anti–IL-12p35). Cells were collected at 0, 4, 12, 24, 48, 72, 96, and 120 hours after culture. mRNA for T-bet was quantified by real-time PCR (TaqMan) and normalized to ubiquitin. Data are representative of 3 independent experiments. (C) At 96 hours, IL-17– and IFN-γ–producing CD4⁺ T cells were identified by intracellular cytokine staining. T-bet and TIM3 expression were determined by costaining of cytokine-positive cells for T-bet (clone 4B10) or TIM3 (clone 8B.2C12).