ArticleTranslational lung cancer research2026
Targeting NLRP3 inflammasome: a novel strategy for improving immune checkpoint inhibitor-associated pneumonitis.
Article in Translational lung cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Umbrella Systematic Review of the Efficacy and Safety of PD-1 Inhibitors Combined with CTLA-4 Inhibitors in the Treatment of Melanoma.International journal of molecular sciences · 2026Pooled it
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment but are frequently accompanied by immune-related adverse events (irAEs) affecting multi-organ. Checkpoint inhibitor-associated pneumonitis (CIP) is a serious irAE whose mechanistic underpinnings remain poorly understood, limiting the clinical application of ICIs. The objective of this study was to investigate the role of the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome in the pathogenesis of CIP and to explore potential targeted therapies. Methods: A CIP mouse model was established via regulatory T cell (Treg) depletion and anti-programmed cell death protein 1 (PD-1) antibody treatment. Lung tissue gene expression was analyzed using RNA-sequencing, quantitative polymerase chain reaction (qPCR), and Western blot. Therapeutic interventions with NLRP3 inflammasome inhibitors (MCC950 and dapansutrile) and a macrophage-depleting agent (clodronate liposomes) were evaluated by micro-computed tomography (CT), histopathology, and serum inflammatory cytokine assays. Validation was performed via single-cell transcriptomic analysis of bronchoalveolar lavage fluid from 13 non-small cell lung cancer patients with or without ICI-induced CIP. Results: The findings revealed: (I) significant upregulation of NLRP3 inflammasome pathway-related genes and downstream factors (IL-1β, IL-18) in CIP mouse lungs, alongside increased macrophage infiltration; (II) pneumonitis injury was markedly alleviated and serum inflammatory cytokine levels were reduced by both NLRP3 inflammasome inhibition and macrophage depletion; (III) dapansutrile downregulated NLRP3 expression via inhibition of the NF-κB pathway; (IV) enriched macrophage subpopulations (Mac-IL1B) expressing high levels of NLRP3 were identified in CIP patients. Conclusions: This study provides the first evidence that NLRP3 inflammasome activation constitutes a key upstream mechanism in CIP pathogenesis, offering novel therapeutic strategies for targeted intervention.
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