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Activation of the P2RX7/IL-18 pathway in immune cells attenuates lung fibrosis.
ELife 2024 Februrary 2
Idiopathic pulmonary fibrosis (IPF) is an aggressive interstitial lung disease associated with progressive and irreversible deterioration of respiratory functions that lacks curative therapies. Despite IPF being associated with a dysregulated immune response, current antifibrotics aim only at limiting fibroproliferation. Transcriptomic analyses show that the P2RX7/IL18/IFNG axis is downregulated in IPF patients and that P2 R X7 has immunoregulatory functions. Using our positive modulator of P2 R X7, we show that activation of the P2 R X7/IL-18 axis in immune cells limits lung fibrosis progression in a mouse model by favoring an antifibrotic immune environment, with notably an enhanced IL-18-dependent IFN-γ production by lung T cells leading to a decreased production of IL-17 and TGFβ. Overall, we show the ability of the immune system to limit lung fibrosis progression by targeting the immunomodulator P2 R X7. Hence, treatment with a small activator of P2 R X7 may represent a promising strategy to help patients with lung fibrosis.
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