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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 1. Poly I:C augments Nod2 activation via TRIF- and IPS-1-dependent signaling pathways in macrophages.

Figure 1

(A–D) BMDMs from WT and indicated mutant mice were left untreated (−) or pretreated with LPS (A), pam3CSK4 (A), or poly I:C (A–D) 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. (E) BMDMs from WT and Trif−/−Ips1−/− mice were treated with poly I:C or left untreated for 24 h. The macrophages were then re-stimulated with MDP. Cell-free supernatants were analyzed by ELISA for production of IL-6 and TNF-α. (*** p < 0.001, compared with untreated and poly I:C-treated or WT and mutant macrophage cultures). N.D. denotes not detected. Results are representative of 2 or 3 independent experiments. Data are expressed as mean ± S.D.

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