Interleukin‐33 Promotes Interstitial Lung Disease in Idiopathic Inflammatory Myopathy Via ERK ‐Mediated Epithelial‐Mesenchymal Transition: ERK as a Potential Therapeutic Target
Authors' conclusion
IL-33 promotes IIM-ILD progression by activating ERK-mediate EMT, identifying the IL-33/ERK signaling axis as a potential therapeutic target.
Study context
- Population
- Patients with IIM-ILD and healthy controls; Myositis-associated ILD (MAILD) mouse model; A549 alveolar epithelial cells
Methodological detailshuman IIM-ILD samples, MAILD mouse model with IL-33 knockout (KO) and reconstitution, in vivo ERK inhibition with U0126, in vitro IL-33 knockdown alveolar epithelial cells challenged with neutrophil extracellular traps (NETs)
- Human IIM-ILD samples
- MAILD mouse model with IL-33 KO and reconstitution
- In vivo ERK inhibition with U0126
- In vitro IL-33 knockdown alveolar epithelial cells challenged with NETs
Main finding
As reported in the abstract
- Serum IL-33 significantly elevated in IIM-ILD vs healthy controls, with concurrent upregulation of IL-33 in lung tissues
- MAILD mice showed increased IL-33 expression; IL-33 KO mice had attenuated lung inflammation, improved alveolar architecture and decreased collagen deposition
- Exogenous IL-33 restored interstitial lung disease (ILD) severity in IL-33 KO mice to wild-type levels
- p-ERK and epithelial-mesenchymal transition (EMT) markers (E-Ca and α-smooth muscle actin) correlated with IL-33 expression
- U0126 reduced p-ERK, suppressed EMT and ameliorated pulmonary inflammation and fibrosis
- In vitro, NETs induced EMT and ERK activation in A549 cells, abolished upon IL-33 silencing
Original publication
Interleukin‐33 Promotes Interstitial Lung Disease in Idiopathic Inflammatory Myopathy Via ERK ‐Mediated Epithelial‐Mesenchymal Transition: ERK as a Potential Therapeutic Target. Arthritis Rheumatol. Published 3 February 2026. doi:10.
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