Fig. 5: E-TMED10 interaction is required for E-induced inflammation.

a Amino acid sequence and domains of the SARS2-E protein. The C-terminal region of SARS2-E (ECT) used to block E-TMED10 interaction is highlighted in orange. b Co-IP using HEK293T cells with TMED10-V5 and Myc-tagged E-SARS2 in the absence or presence of GFP or GFP-tagged CT of E-SARS2 (GFP-ECT). c mIL1β-HA secretion in HEK293T cells transfected with or without Myc-tagged E-SARS2, or in the absence or presence of GFP or increasing amount of GFP-ECT. d THP-1 cells were expressed with GFP or GFP-ECT followed by differentiation and mIL1β secretion determination. e Crosslink assay performed using HEK293T cells expressing TMED10-V5 in the absence or presence of Myc-E-SARS2, GFP or GFP-ECT as indicated. f Cell-free membrane translocation of mIL1β-FLAG in the absence or presence of Myc-E-SARS2 and cytosol in the presence of GFP or GFP-ECT as indicated. g–j C57BL/6 mice co-injected with AAV-Myc-E-SARS2 and AAV-GFP or AAV-GFP-ECT were challenged with LPS and euthanized. Expression of Myc-E-SARS2, GFP, GFP-ECT in the lung were verified by IF (i, left panel). Serum IL1β levels were determined by ELISA (g). IL6 mRNA levels in indicated tissues were analyzed in (h). Lung inflammation was analyzed by H&E staining (i, right panel) and inflammatory area was quantified in (j). Prot K, Protease K; TX-100, TritonX-100. Data are mean ± s.d. Statistical significance was assessed using two-tailed t test (n = 5). P values are indicated. Scale bars, 50 μm. Source data are provided as a Source Data file.