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. Author manuscript; available in PMC: 2015 Jun 15.
Published in final edited form as: J Immunol. 2014 May 7;192(12):5548–5560. doi: 10.4049/jimmunol.1400122

Figure 5. Caspase-8-deficient DCs are hyper-responsive to TLR activation in a RIPK1-dependent manner.

Figure 5

(A) GM-CSF + Flt3-L-treated BMDCs from Casp8fl/fl (control) and CreCD11cCasp8fl/fl mice were stimulated with imiquimod ± Nec-1 and/or zIETD-FMK (zIETD) and/or 1-Methyl-D-tryptophan (1-MT) for 6 hours ± ATP (5mM) and supernatants evaluated for IL-12/IL-23p40, IL-6, TNFα, and IL-1β. (B–C) 3-month-old control and CreCD11cCasp8fl/fl mice (n=4) injected with imiquimod (200 µg/mouse) or PBS were evaluated 4 hours later for splenic CD11c+CD8− conventional DC CD86, MHCII, and CD40 expression, represented as the fold change over PBS injection. Data are represented as mean ± SD and compared by Mann Whitney test: *, p<0.05; **, p<0.005; ***, p<0.0005.