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. Author manuscript; available in PMC: 2020 Jun 30.
Published in final edited form as: Cell Rep. 2020 May 5;31(5):107604. doi: 10.1016/j.celrep.2020.107604

Figure 3. Splenic DCs Suppress Inflammasome Activation and Prime T Cells in Response to Virulent Pathogens.

Figure 3.

(A) OT-II and OT-I T cell proliferation was quantified by flow cytometry following 72 h of culture with WT CD11c+ splenic DCs that were pulsed with STm or STmΔspi1 in and OVA.

(B) IL-2 was measured by ELISA in the supernatants of the cultures from (A).

(C) Immunoblot analysis of pro-casp1 (p45) and cleaved casp1 (p20) in the lysates of WT BMDCs and CD11c+ splenic DCs pulsed with STm or STmΔspi1 for 1 h.

(D and E) IL-1β was measured by ELISA (D), and (E) cell death was measured by LDH release in the supernatants of WT BMDCs and CD11c+ splenic DCs from (C).

(F) OT-II T cell proliferation was quantified by flow cytometry following 72 h of culture with FACS-sorted GM-Macs (CD11c+MHCIIintCD115+) and GM-DCs (CD11c+MHCII+CD115−) that were pulsed with STm and OVA.

(G) Immunoblot analysis of pro-casp1 (p45) and cleaved casp1 (p20) in the lysates of FACS-sorted GM-Macs and GM-DCs pulsed with STm for 1 h.

(H) IL-1β was measured by ELISA in the supernatants of GM-Macs and GM-DCs from (G).

See also Figures S1 and S2. Error bars indicate SEM; (A, B, D–F, and H) paired t test; (C and G) data representative of three independent experiments. *p<0.05, **p<0.01, ***p<0.001; ns, not significant.