Type 2 dendritic cells (DC2s) are essential for TH2 differentiation, but the signaling pathways involved in allergen sensing, DC activation and instruction of CD4+ T cell priming remain unclear. Previous transcriptomic analyses demonstrated a type-I interferon (IFN-I) signature in skin cDC2s following immunization with non-viable larvae ofNippostrongylus brasiliensis(Nb), house dust mite (HDM), andSchistosomaegg antigen (SEA). Blocking IFN-I signaling with anti-IFNAR1 (aIFNAR1) led to reduced TH2 cytokine responses to these antigens, however, the phenotype of cytokine-producing CD4+ T cells was not further defined. Here we show that conditional loss of IFNAR1 signaling in CD11c+ DCs significantly impaired effector TH2 and TFH CD4+ T cell responses toNb.In vivoproliferation experiments demonstrated reduced numbers of highly divided CD4+ T cells in IFNAR1ΔCD11cmice compared to IFNAR1WT, with the highly divided population comprising both TH2 and TFH. Characterization of the cDC2 compartment by flow cytometry and bulk RNAseq demonstrated lower numbers ofNb+ cDC2s in the skin-draining LN and a reduced expression ofIl15andIl15Rain IFNAR1ΔCD11cmice compared to IFNAR1WT, while expression of costimulatory molecules including CD80, CD86,Cd40andPdcd1lg2(PD-L2) was not impaired. Therefore, IFN-I conditioning of skin cDC2s is necessary for their effective priming of CD4+ T cell responses to allergens, providing evidence for a role of tissue cytokines in driving cDC2 activation in a TH2 context.