Extended Data Fig. 1: Activity and expression of BTN3A1 and BTN3A3 in cell lines and human tissues.

a, siRNA knock-down of BTN3A1 in MRC5T and hBEC3-KT. Cells were transfected with scrambled (Neg ctrl) or BTN3A1-targeting siRNAs, and protein levels in the resulting cell lysates were assessed by western blotting. α-Tubulin was used as loading control. Arrows indicate the band corresponding to BTN3A1. For gel source data, see Supplementary Fig. 1. b, Graphs showing the replication kinetics of PR8 and Mallard in siRNA-treated MRC5T and hBEC3-KT cells. Cells were infected with a MOI of 0.001, supernatants were collected at the indicated times post infection and viruses titrated by plaque assay. Data are mean +/− SEM of 3 independent experiments (each using 2 technical replicates). Statistical significance between groups was measured by a 2-way ANOVA. Comparisons were made between area under the curve of the different BTN3A1 siRNA treatment conditions and the average of the two negative controls. No statistically significant differences were found. c, Organ-dependent bulk tissue gene expression. Lung samples are highlighted in blue. d, Lung single cell tissue expression. Data in c and d were obtained from the GTEx Portal (www.gtexportal.org). e, Western blotting of cell lysates obtained from A549, MRC5T, hBEC3-KT and Calu-3 treated with either IFN-γ or universal type-I IFN. Treatment with IFN was for 16h in A549, MRC5T, hBEC3-KT and for 24h in Calu-3 cells. pSTAT1 and RSAD2/Viperin were used as IFN induction controls and α-Tubulin as loading control. For gel source data, see Supplementary Fig. 1.