IL17A and pulmonary fibrosis: GO analysis of these genes revealed perturbation of “immune response,” “extracellular matrix organization,” and “collagen metabolism” biological processes as well as enrichment of “ECM-receptor interaction,” “cytokine-cytokine receptor interaction,” “chemokine,” and “IL-17” signaling pathways (Figure 3A and Supplementary Figures 6, 7), reflecting ongoing inflammatory immune responses in both IPF and SSc-PF, even at such a late stage of pulmonary fibrosis.