The type I IFN induction pathway constrains Th17-mediated autoimmune inflammation in mice
J. Clin. Invest. Beichu Guo, et al. 118:1680 doi:10.1172/JCI33342 [Go to this article.]

Figure 3
Th17 development in TRIF-deficient mice. (A) Flow cytometry analysis of CNS mononuclear cells from WT and TRIF-deficient mice at day 21 after immunization. CNS mononuclear cells isolated from WT and TRIF^–/– mice were stained for intracellular IL-17. Plots were gated on CD4⁺ T cells. Numbers indicate percentage of IL-17⁺CD4⁺ cells of total CD4⁺ cells. (B) T cells from TRIF-deficient mice immunized with antigen were hyperresponsive ex vivo. Total splenocytes were isolated from WT and TRIF-deficient mice 7 days after immunization and restimulated with MOG peptide ex vivo for 3 days. IL-17 production was measured by ELISA. (C and D) Ex vivo response of splenocytes from WT and TRIF-deficient mice 21 days after immunization. IL-17 or IFN-γ production was measured by ELISA. Results are reported as mean ± SD of duplicate samples from 1 representative experiment of 3 independent experiments.