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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 1. MYD88 and TLRs are associated with the severity of COVID-19.

Figure 1.

(A–J) Absolute RNA counts of MYD88 (A), TRIF (B), TLR1 (C), TLR2 (D), TLR3 (E), TLR4 (F), TLR5 (G), TLR7 (H), TLR8 (I), and TLR9 (J) in patients with mild-to-moderate (n = 11), severe (n = 10), and critical (n = 11) COVID-19, and 13 healthy controls16. (K) Immunoblot analysis of phospho-ERK (pERK), total ERK (tERK), pIκB, and tIκB in WT, Myd88–/–, and Trif–/– bone marrow-derived macrophages (BMDMs) after infection with MHV at a MOI of 0.1 for the indicated time. Actin was used as the internal control. (L) Real-time PCR analysis of Tnf expression in WT, Myd88–/–, and Trif–/– BMDMs after infection with MHV at a MOI of 0.1 for the indicated time, presented relative to levels of the host gene Gapdh. Significant differences compared to the healthy group are denoted as *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001; ns: not significant (one-way ANOVA). Exact P values are presented in Supplementary Table 1. Data are shown as mean ± SEM (A–J, L). Data are representative of three independent experiments (K and L).