Although our data showing TGF-β1 suppression of CCL8 production by in vitro–stimulated macrophages supports such a direct mechanism, it remains possible that the likely monocyte origin of the majority of SigF+ AM-like cells in these mice endows them with greater capacity for CCL8 production, as was recently demonstrated for IL-6 in monocyte-derived AMs during influenza infection.19 Here, CCL8 is linked to influenza.