Overall, it is plausible to suggest that the impact of CD11c+ DC PLXND1 KO on airway remodelling and fibrosis could be mediated either by direct interaction of CCL-2/MCP-1 with fibroblasts/myofibroblasts or indirectly by increased recruitment of interstitial macrophages (i.e., M2 macrophages) into the lung, which is associated with pulmonary fibrosis [68]. This evidence concerns the gene ITGAX and pulmonary fibrosis.