CXCL9 and pulmonary fibrosis: During lung fibrosis, pneumonocytes and adjacent fibroblasts enriched in the fibrotic wound express the chemokine CXCL9 and its receptor CXCR3; CXCL9 signaling activates Smad7 and suppresses TGFβ signaling in lung epithelial cells, thus providing a mechanism that counterbalances the pro-EMT and pro-fibrotic action of TGFβ in the lung [78].