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. Author manuscript; available in PMC: 2011 Jun 9.
Published in final edited form as: Nat Immunol. 2010 Mar 28;11(5):385–393. doi: 10.1038/ni.1859

Figure 1.

Figure 1

Disruption of mouse Aim2 abolishes activation of the inflammasome by cytoplasmic DNA and vaccinia virus. (a) Immunoblot analysis of the expression of AIM2 in spleens and BMDMs from Aim2+/+ and Aim2−/− littermates (top) and in spleens from Aim2−/−, Aim2+/+ and Aim2+/− mice (bottom), assessed with an antibody specific for mouse AIM2. β-actin serves as a loading control. (b) Immunoblot (IB) analysis of mouse procaspase-1, caspase-1 (p20 subunit) and/or AIM2 in culture supernatants (Sup) and lysates (Lys) of Aim2+/+ and Aim2−/− BMDMs left untreated (None) or transfected with the synthetic DNA poly(dA:dT) or plasmid DNA (pcDNA), or treated for 5 h with LPS (500 ng/ml) followed by nigericin (2.5 µM) for 45 min (LPS + nig), assessed with monoclonal antibody to mouse caspase-1 p20 (anti-p20). (c) Release of LDH into culture supernatants of the BMDMs described in b, presented relative to the total cellular LDH content. *P < 0.05 and **P < 0.01, Aim2+/+ versus Aim2−/− (Student’s t-test). (d) Immunoblot analysis of mouse procaspase-1 and caspase-1 in culture supernatants and lysates of mouse Aim2−/− and Aim2+/+ BMDMs infected for 18 h with vaccinia virus (multiplicity of infection (MOI), above lanes). Data are representative of at least three experiments (mean and s.d. in c).