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. 2020 Feb 4;9:e49416. doi: 10.7554/eLife.49416

Figure 4. Decreased IRF4 expression in cDC2s promotes pro-Th17 phenotype.

(A) IRF4 expression in the Irf4i cDC2s treated with or without doxycycline (Dox, 200 ng/ml) for 16 hr. (B–D) IL-17A, IL-5 and IFN-γ levels and (E) T cell lineage commitment factors from the re-stimulated OT-II cells co-cultured with cDC2s from WT and Irf4i mice under the conditions described above. (F) IL-17A levels from anti-CD3/28 Ab-stimulated OT-II cells co-cultured with IRF4ΔCD11c cDC2s. (G) IL-1β and (H) IL-6 level in WT and IrfΔCD11c cDC2s after treatment of CPT or Curdlan for 24 hr. Data are representative of three independent experiments; *p<0.05, **p<0.01. (I) A schematic diagram of Th2 inhibition and pro-Th17 induction by PRR-independent and -dependent signals.

Figure 4.

Figure 4—figure supplement 1. Decreased IRF4 expression in BM-APCs promotes pro-Th17 phenotype and sustained IRF4 expression blocks cAMP-induced Th17 bias.

Figure 4—figure supplement 1.

(A) IRF4 expression in the WT and Irf4i BM-APCs treated with or without doxycycline (Dox, 200 ng/ml) for 16 hr. After the Dox treatment cells were washed and treated with CPT (50 μM) for 48 hr. (B, C) IL-17A and IL-5 levels from the re-stimulated OT-II cells co-cultured with BM-APCs from WT and Irf4i mice under the conditions described above. Data are mean ± s.e.m, n = 3 in each group; *p<0.05, # p<0.05 compared to WT untreated.
Figure 4—figure supplement 2. Loss of IRF5 in cDC2s inhibited CPT induced pro-Th17 phenotype.

Figure 4—figure supplement 2.

(A) IL-17A levels from anti-CD3/28 Ab-stimulated OT-II cells co-cultured with CPT-treated cDC2s from WT and Irf5-/- mice. (B) QPCR of TFs in CPT-treated WT and Irf5-/- cDC2s. Data are representative of three independent experiments; *p<0.05.