ArticleProceedings of the National Academy of Sciences of the United States of America2024
The TOX-RAGE axis mediates inflammatory activation and lung injury in severe pulmonary infectious diseases.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Engineering an immune-integrated lung-on-a-chip to reveal TOX-RAGE axis-driven fibrosis and RAGE blockade as a therapeutic strategy.Nano convergence · 2025Article
- Early-life human CD8Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Methylglyoxal is an antibacterial effector produced by macrophages during infection.Cell host & microbe · 2025Article
- Mass Spectrometry Imaging: Revolutionizing Molecular Insights in Infectious Diseases Research.Pathogens (Basel, Switzerland) · 2025Review
- PRMT1 Ablation in Endothelial Cells Causes Endothelial Dysfunction and Aggravates COPD Attributable to Dysregulated NF-κB Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- T-cell exhaustion in COVID-19: what do we know?Frontiers in immunology · 2025Review
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Authors and funding
14 authors.
Funding
Abstract
Thymocyte selection-associated high-mobility group box (TOX) is a transcription factor that is crucial for T cell exhaustion during chronic antigenic stimulation, but its role in inflammation is poorly understood. Here, we report that TOX extracellularly mediates drastic inflammation upon severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection by binding to the cell surface receptor for advanced glycation end-products (RAGE). In various diseases, including COVID-19, TOX release was highly detectable in association with disease severity, contributing to lung fibroproliferative acute respiratory distress syndrome (ARDS). Recombinant TOX-induced blood vessel rupture, similar to a clinical signature in patients experiencing a cytokine storm, further exacerbating respiratory function impairment. In contrast, disruption of TOX function by a neutralizing antibody and genetic removal of RAGE diminished TOX-mediated deleterious effects. Altogether, our results suggest an insight into TOX function as an inflammatory mediator and propose the TOX-RAGE axis as a potential target for treating severe patients with pulmonary infection and mitigating lung fibroproliferative ARDS.
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