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 4
Type I IFN induction pathway in innate immune system constrains the development of Th17 development and CNS autoimmune disease. (A) Adoptive transfer experiments. Spleen cells and draining lymph node cells isolated from immunized WT mice were used as donor cells and restimulated with 20 μg/ml of MOG peptides in vitro. 3 × 10⁷ cells were transferred into WT or TRIF^–/– naive recipient mice via tail-vein injection (5 mice per group). The mice were monitored daily for clinical signs of disease. (B) Spleen cells and draining lymph node cells isolated from immunized TRIF^–/– mice were restimulated with MOG peptide in vitro for 72 hours. 3 × 10⁷ cells were transferred into WT or TRIF-deficient naive recipient mice via tail-vein injection (5 mice per group). (C) Flow cytometry analysis of Th17 development in CD4⁺ T cells cocultured with BMMs. BMMs from WT mice, TRIF-deficient, or IFNAR-deficient mice were stimulated with LPS (100 ng/ml) for 24 hours, then were cultured with WT naive CD4⁺ T cells in the presence of anti-CD3 (1 μg/ml) for 72 hours. Cells were stained for surface CD4 and intracellular IL-17. Plots were gated on CD4⁺ T cells. Numbers indicate percentage of IL-17⁺CD4⁺ cells of total CD4⁺ cells. (D) IL-17 production in the coculture of WT CD4⁺ T cells and BMMs in experiments described in C. (E) IL-17 production from TRIF-deficient CD4⁺ T cells cocultured with BMMs.