ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025
IFN-γ-mediated suppression of Caspase-7 exacerbates acute lung injury induced by CAR-T cells.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Novel CAR T cell blend targeting PDPN and GD2 to overcome glioblastoma heterogeneity.Journal for immunotherapy of cancer · 2026Article
- In vivo CAR-cell therapy: current challenges and emerging therapeutic advances.Molecular biomedicine · 2026Review
- Erythrocyte membrane-liposome coating sustains circulation stability and targeted tumor therapy of CAR-T cells.Frontiers in immunology · 2026Article
- Review
- Avoiding the toll of lung injury while driving CAR T cells to the target tumor.Journal of thoracic disease · 2025Article
- EF1α, rather than CMV promoter, is suitable for luciferase tag expression in target cells forMolecular therapy. Methods & clinical development · 2025Article
- Enhanced homing and efficacy of HER2-CAR T cells via CXCR5/CCR6 co-expression for HER2-positive NSCLC.Journal of translational medicine · 2025Article
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13 authors.
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Abstract
On-target off-tumor effects precipitate severe adverse reactions in patients, significantly hindering the application of chimeric antigen receptor (CAR) T cells in both hematological and solid tumors. The underlying mechanisms remain elusive due to the absence of suitable preclinical models. To elucidate these mechanisms, a human epidermal growth factor receptor 2 (Her2) transgenic mouse model was developed to investigate CAR-T cell-induced on-target off-tumor effects. CAR-T cells initially migrated to the lungs, targeting alveolar epithelial cells and resulting in interferon-γ (IFN-γ)-dependent acute lung injury. Additionally, a regulatory mechanism involving IFN-γ-induced degradation of caspase-7 mRNA 5' untranslated regions (UTR), which amplifies acute lung injury mediated by CAR-T cells, was identified. Consequently, a strategy was validated to antagonize IFN-γ during CAR-T cell infusion, thereby mitigating acute lung injury without compromising antitumor efficacy. These findings elucidate the mechanisms of CAR-T cell-induced acute lung injury and demonstrate the viability of targeting IFN-γ to prevent this adverse reaction.
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