Fig. 2

Plasmodium gDNA activates innate immune AIM2 inflammasome, while RNA and hemozoin trigger NLRP3 inflammasome activation. a WT and Casp1^−/− mice (n = 5) were infected with P. yoelii YM, and splenocytes were harvested at 18 h after infection. Uninfected samples served as control group. Cell lysates were analyzed by immunoblotting with the indicated antibodies. b, c WT pDCs were stimulated as indicated for 24 h, cell lysate and supernatants were collected for immunoblotting analysis (b), and supernatants were collected for quantization of IL-1β cytokine by ELISA analysis (c). d, e WT peritoneal macrophages (d) and cDCs (e) were stimulated as indicated for 24 h, and supernatants were collected for quantization of IL-1β cytokine by ELISA analysis. f, g LPS-primed WT, Il1r1^−/−, Aim2^−/−, Nlrp3^−/− and Casp1^−/− pDCs were stimulated with gDNA (f) or RNA (g) for 24 h, and supernatants were collected for quantization of IL-1β cytokine by ELISA analysis. h WT, Il1r1^−/−, Aim2^−/−, Nlrp3^−/−, and Casp1^−/− pDCs were stimulated with gDNA/hemozoin complex for 24 h, supernatants were collected for quantization of IL-1β cytokine by ELISA analysis. Data are representatives of three independent experiments with similar results and plotted as mean ± SD. *p < 0.05, **p < 0.01 vs. corresponding control. NS, not significant