Figure 1.

Inhibition of individual pattern recognition receptor (PRR) signaling pathways implicates the involvement of retinoic acid-inducible gene-I-like receptor (RLR) and C-type lectin receptor (CLR) for the immune activation in Middle East respiratory syndrome coronavirus (MERS-CoV)-infected macrophages. (A) The inhibitors for various PRR signal pathways, the 50% cytotoxic concentration (CC₅₀), and the working concentration used in the study are listed. (B) The MERS-CoV-infected monocyte-derived macrophages (MDMs) were treated with the inhibitors or mock-treated in triplicate. At 24 hours postinfection, cells were lysed for detecting messenger ribonucleic acid expression levels of proinflammatory cytokines and chemokines. Results show the fold change of glyceraldehyde 3-phosphate dehydrogenase-normalized expression level in the treated or mock-treated cells relative to that in the mock-infected cells. Data are presented as mean ± standard deviation of triplicate wells of MDMs from 3 different donors. Unpaired t test was used for data analysis. *, P < .05; **, P < .01; ***, P < .001. IFN, interferon; IKKε, inhibitor of NF-κB kinase epsilon; IL-6, interleukin 6; MIP, macrophage-inflammatory protein; NLR, nucleotide-binding oligomerization domains-like receptor; Syk, spleen tyrosine kinase; TBK1, TANK-binding kinase 1; TNF, tumor necrosis factor.