Previous studies have shown that populations of lung-fibrotic fibroblasts (expressing JUN and IL6 with upregulation of the immune-checkpoint proteins CD47 and PDL1) and immunosuppressive PD1+ macrophages (expressing IL1β) are involved in impaired alveolar regeneration and a weakened adaptive T cell immune response during pulmonary fibrosis in humans and mice, as well as during SARS-CoV-2 infection [18, 19, 21, 59]. Here, IL1B is linked to pulmonary fibrosis.