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. Author manuscript; available in PMC: 2012 Jun 16.
Published in final edited form as: Cell Host Microbe. 2011 Jun 16;9(6):496–507. doi: 10.1016/j.chom.2011.05.006

Figure 2. Enhancement of Nod2 signaling by poly I:C and the chemotherapeutic molecule DMXAA is mediated via type-I IFNs.

Figure 2

(A and C) BMDMs from WT and Ifnar1−/− mice were left untreated (control) or pretreated with poly I:C (A), DMXAA, or IFN-β (C) for 24 h and then restimulated with MDP. Cell extracts were collected at the indicated times and assessed for MAPK and NF-κB activation using phosphospecific antibodies. (B and D) BMDMs from WT, Ifnar1−/− (B), or Nod2−/− mice (D) were treated with poly I:C, DMXAA, or left untreated for 24 h and then re-stimulated with MDP. Cell-free supernatants were analyzed for production of IL-6 and TNF-α (*** p < 0.001, compared with WT and mutant macrophage cultures). N.D. denotes not detected. Results are representative of 3 independent experiments. Data are expressed as mean ± S.D.

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