These invasive fibroblasts expressed high levels of immune checkpoint ligands Cd274 (PDL1) and Pdcd1lg2 (PDL2), semaphorin 7A (CD108), Itga6 (CD49f) and F3 (CD142), and functional in vitro experiments showed that HER2 inhibition ameliorated lung fibrosis, especially when combined with anti-PDL1 treatment. This evidence concerns the gene PDCD1LG2 and pulmonary fibrosis.