Priming of pathogenic MOG_35–55-specific CD4⁺ T cells is increased in LNs of mice lacking MHCII expression by pDCs. (A) Effector MOG_35–55-specific CD4⁺ T cells were generated from 2D2 mice and adoptively transferred into WT:WT and pIII+IV^−/−:WT chimeras. Results are representative of two experiments. The means and SEM derived from four mice per group are shown. (B) Effector MOG_35–55-specific CD4⁺ T cells were generated from MOG_35–55-immunized WT:WT or pIII+IV^−/−:WT chimeras and adoptively transferred into WT mice. Results show the mean and SEM derived from two experiments with a total of seven or eight mice per group. *, P < 0.05. (C–E) EAE was induced by immunization with MOG_35–55+CFA in WT:WT and pIII+IV^−/−:WT chimeras. dLN cells isolated 9 and 14 d after immunization were restimulated in vitro with MOG_35–55 and analyzed by flow cytometry for the expression of CD4, IFN-γ, and IL-17. (C) Representative flow cytometry profiles analyzing IFN-γ and IL-17 expression by CD4⁺ T cells are shown. Percentages of CD4⁺ T cells expressing IFN-γ and IL-17 are indicated. (D and E) Histograms represent the percentages of CD4⁺ T cells expressing IFN-γ (D) or IL-17 (E). Results show the mean and SEM derived from two independent experiments with at least three mice per group. *, P < 0.05; **, P < 0.01. (F) Concentrations of IFN-γ, IL-17, IL-4, and IL-10 were measured in culture supernatants from MOG_35–55-restimulated LN cells isolated 14 d after induction of EAE. Results show the means and SEM derived from two independent experiments, each with at least three mice per group. ns, not significant; *, P < 0.05; **, P < 0.01.