We, for the first time, demonstrate that TGF-β1 released from MSCs may block myofibroblast activation in CTD-UIP HLFs through sensitizing the TGFβ/Smad signaling pathway that is severely attenuated by excessive IL-6/STAT3 signaling, thereby overcoming the proinflammatory phenotype and relieving the inhibition of IP-10 expression to push against myofibroblast differentiation. Here, IL6 is linked to idiopathic pulmonary fibrosis.