To confirm the robustness of the BMDM2 phenotype outside of its local (inflammation-resolving) microenvironment, we developed a short-term infection model and applied in vivo-generated BMDM2 (vs. BMDM1) by intrapulmonary transfer into IAV-infected Ccr2-/- mice) lacking BM-monocyte mobilization and BMDMs in inflamed tissues8, in an effort to prevent severe injury peaking at D7 (Fig. 3g). This evidence concerns the gene CCR2 and infection.