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. Author manuscript; available in PMC: 2022 Feb 27.
Published in final edited form as: Nat Immunol. 2021 May 7;22(7):829–838. doi: 10.1038/s41590-021-00937-x

Figure 2. TLR2 is required for the inflammatory response during β-coronavirus infection.

Figure 2.

(A–C) Real-time PCR analysis of the expression of Il1b (A), Il6 (B), and Tnf (C) in WT, Tlr2–/–, Tlr4–/–, Tlr7–/–, and Tlr9–/– bone marrow-derived macrophages (BMDMs) after infection with MHV at a MOI of 0.1 for the indicated time, presented relative to levels of the host gene Gapdh. (D) Immunoblot analysis of phospho-ERK (pERK), total ERK (tERK), pIκB, and tIκB in WT, Tlr2–/–, and Tlr7–/– BMDMs after infection with MHV at a MOI of 0.1 for the indicated time. GAPDH was used as the internal control. (E–L) TNF-α (E), IFN-γ (F), IL-1α (G), IL-6 (H), CXCL10 (I), MCP-1 (J), G-CSF (K), and CCL3 (L) release from human peripheral blood mononuclear cells (PBMCs) infected with SARS-CoV-2 at a MOI of 0.5 for 20 h with or without the TLR2 inhibitor (oxPAPC; TLR2 in) or TLR4 inhibitor (CLI-095; TLR4 in). Significant differences compared to the media control infection group are denoted as *P < 0.05 and ***P < 0.001; ns: not significant (one-way ANOVA) (E–L). Exact P values are presented in Supplementary Table 1. Data are representative of three independent experiments (A–D) or two independent experiments (E–L). Data are shown as mean ± SEM (n = 3 biological replicates) (A–C and E–L).