Fig. 6
Negative regulator SOCS1 is directly induced by IL-1β signaling in a MyD88-TRAF3-IRF3-dependent type I IFN signaling. a, b WT and Il1r1−/− mice (n = 5) were infected with P. yoelii YM for indicated times, and RNA from splenocytes was isolated and used for expression analysis of Socs1 (a), Ifna and Ifnb (b) by using qPCR. c WT pDCs were stimulated with recombinant mouse IL-1β (2 μg/ml) for indicated times, RNA from the pDCs was isolated and used for expression analysis of Socs1 by using qPCR. d WT, Il1r1−/−, Myd88−/−, and Irf3−/− pDCs were stimulated with recombinant IL-1β (2 μg/ml) for indicated times, RNA from pDCs was isolated and used for expression analysis of Socs1 by using qPCR. e WT and Traf3f/f CD11c-cre pDCs were stimulated with recombinant IL-1β (2 μg/ml) for indicated times, RNA from pDCs was isolated and used for expression analysis of Socs1 by using qPCR. f–h WT, Traf3f/f CD11c-cre, and Traf3f/wt CD11c-cre mice (n = 5) were infected with P. yoelii YM. Serum was collected at 24 h post infection and subjected to ELISA analysis for IFN-α, IFN-β (f). Parasitemias (g) and survivals (h) were monitored daily. i A model to show whether SOCS1 is directly induced by IRF3-dependent signaling or the downstream IFNAR-mediated signaling. j WT and Irf3−/− cDCs were pretreated with or without anti-IFNAR antibody for 24 h and stimulated with YM gDNA plus RNA for indicated times. RNA from cDCs was isolated and used for expression analysis of Socs1 by using qPCR. k, l WT and Stat1−/− cDCs were stimulated with YM gDNA plus RNA (k) or mouse IFN-α/β (l) for indicated times. RNA from splenocytes was isolated and used for expression analysis of Socs1 by using qPCR. Data are representative of three independent experiments and plotted as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001 vs. corresponding control. NS, not significant. Dagger denotes mouse death
