Consistent with increased lymphocyte activation, the predicted frequency of global pro-inflammatory cell–cell interactions was increased in the aged lung (Fig. 2f, g; Supplementary information, Fig. S4e and Table S5), approximately half of which were related to cytokine production and leukocyte activation (e.g., TNFSF10, TNFSF13, IL1A, IL15RA, as well as TGF-β1 and TGF-β2, master regulators of lung fibrosis) (Fig. 2g; Supplementary information, Table S5). Here, IL1A is linked to pulmonary fibrosis.