The role of recruitment versus training in influenza-induced lasting changes to alveolar macrophage function

In their recent publication, Wang et al. propose that influenza infection in the lungs confers resistance to metastatic tumor growth due to trained immunity in the alveolar macrophage (AM) compartment, underpinned by enhanced pro-inflammatory cytokine production, augmented phagocytosis and metabolic rewiring 1 .Although these findings are broadly in line with prior work demonstrating that viral infections can cause long-lasting changes in the AM compartment, affecting subsequent challenges 2-5 , many of these earlier studies attributed functional changes to monocyte-derived AMs emerging during infection 2-4 rather than training of pre-existing AMs.In light of this discrepancy, we believe that there is insufficient consideration of AM origin in the study by Wang et al. to formally claim that the mechanism of tumor protection is trained immunity.We believe that strategies chosen