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. 2014 Oct;28(10):4223–4234. doi: 10.1096/fj.13-247650

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Figure 9. — Model of the crosstalk between compliment activation and TGF-β1 in augmenting epithelial injury. TGF-β1 mediates epithelial injury by down-regulating the CIPs via the p38MAPK/Snail axis in primary normal human SAECs. Both C3a and C5a are capable of down-regulating CIPs, directly and by inducing the p38MAPK/Snail axis. Furthermore, whereas both C3a and C5a effectively suppress SMAD7, only C3a induces TGF-β1 expression. TGF-β1 contributes to the signaling potency of C3a and C5a by up-regulating the expression of their respective receptors. The crosstalk collectively amplifies epithelial injury and tissue damage.