Fig 1: SIDT1 is mediating IFN-I responses to endosomal TLR in mouse pDC.(a) Splenocytes from WT (n = 17) and sidt1-/- (n = 15) mice were stimulated with ODN2216 (CpG), imiquimod (Iq) and resiquimod (Rq). Supernatants were collected at 48 h and assayed for type I IFN and TNFa. NS, non-stimulated (b) BM-pDC from WT (n = 7) and sidt1-/- (n = 6) mice were stimulated for 48h with ODN2216. Top panel, IFN-I and TNFa were quantified as before. Bottom panel, expression of maturation markers monitored by flow cytometry in the SiglecH+ gate, after exclusion of dead cells using DRAQ7. (c) BM-pDC were stimulated as in (b) and the translocation of NF-?B and IRF7 was quantified by image cytometry as in Figure 5. (d) Left, IFN-I levels in the serum of WT (n = 11) and sidt1-/- (n = 8) in untreated (NT) and Aldara (Iq) animals 2 h after treatment. Right, TNFa in serum of the same animals. Pooled animals of at least three independent experiments for (a) and (d) and two independent experiments in (b) and (c). Individual mice data, median and IQR values are plotted * p < .05; ** p < .01 in two-tailed Mann-Whitney tests.