Stress-NRF2 response axis polarizes tumor macrophages and undermines immunotherapy
Our data pinpoint a previously underappreciated cytoprotective mechanism, which inadvertently sustains immunosuppressive macrophages and confers therapy resistance. These results define stress-induced TAMs as an untapped driver of macrophage-based immune evasion. Inhibiting NRF2 activity alongside standard immunotherapies could restore a pro-inflammatory macrophage-T-cell amplification loop, potentially improving patient responses to T-cell-and macrophage-directed immunotherapies.
Authors
- Livio Baselgia (ORCID: https://orcid.org/0000-0003-2583-8195)
- Elena Duerst (ORCID: https://orcid.org/0000-0002-4386-6475)
- Dominik J. Schaer (ORCID: https://orcid.org/0000-0002-6468-4013)
- Nadja Schulthess (ORCID: https://orcid.org/0000-0002-2918-6262)
- Kerstin Hansen
- Rok Humar (ORCID: https://orcid.org/0000-0002-5393-9455)
- Kahrisan Kunasingam
- Melanie Eschment
Institutions
- University of Zurich (CH)
Publication Details
- Journal
- Journal for ImmunoTherapy of Cancer
- Published
- 2025-10-31
- DOI
- https://doi.org/10.1136/jitc-2025-013063
- Citations
- 1
- Primary Topic
- Genomics, phytochemicals, and oxidative stress
- Type
- article
- Field-Weighted Citation Impact
- 0.81
Funders
- National Science Foundation
- Novartis Foundation
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Universität Zürich