Myeloid progenitor dysregulation fuels immunosuppressive macrophages in tumors Article Swipe
Samarth Hegde
,
Bruno Giotti
,
Brian Y. Soong
,
László Halász
,
Jessica Le Bérichel
,
Assaf Magen
,
Benoit Kloeckner
,
Raphaël Mattiuz
,
Matthew D. Park
,
Adam Marks
,
Meriem Belabed
,
Pauline Hamon
,
Theodore Chin
,
Leanna Troncoso
,
Juliana J. Lee
,
Dughan Ahimovic
,
Michael J. Bale
,
Grace Chung
,
Darwin D’souza
,
Krista Angeliadis
,
Travis Dawson
,
Seunghee Kim‐Schulze
,
Raja M. Flores
,
Andrew Kaufman
,
Florent Ginhoux
,
Steven Z. Josefowicz
,
Sai Ma
,
Alexander M. Tsankov
,
Thomas U. Marron
,
Brian D. Brown
,
Miriam Mérad
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1101/2024.06.24.600383
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1101/2024.06.24.600383
Monocyte–derived macrophages (mo-macs) drive immunosuppression in the tumor microenvironment (TME) and tumor-enhanced myelopoiesis in the bone marrow (BM) fuels these populations. Here, we performed paired transcriptome and chromatin analysis over the continuum of BM myeloid progenitors, circulating monocytes, and tumor-infiltrating mo-macs in mice and in patients with lung cancer to identify myeloid progenitor programs that fuel pro-tumorigenic mo-macs. Analyzing chromatin accessibility and histone mark changes, we show that lung tumors prime accessibility for Nfe2l2 (NRF2) in BM myeloid progenitors as a cytoprotective response to oxidative stress. NRF2 activity is sustained and increased during monocyte differentiation into mo-macs in the lung TME to regulate oxidative stress, in turn promoting metabolic adaptation, resistance to cell death, and contributing to immunosuppressive phenotype. NRF2 genetic deletion and pharmacological inhibition significantly reduced mo-macs’ survival and immunosuppression in the TME, enabling NK and T cell therapeutic antitumor immunity and synergizing with checkpoint blockade strategies. Altogether, our study identifies a targetable epigenetic node of myeloid progenitor dysregulation that sustains immunoregulatory mo-macs in the TME.
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Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1101/2024.06.24.600383
- OA Status
- green
- Cited By
- 6
- References
- 105
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4400161714
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4400161714Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1101/2024.06.24.600383Digital Object Identifier
- Title
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Myeloid progenitor dysregulation fuels immunosuppressive macrophages in tumorsWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2024Year of publication
- Publication date
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2024-06-28Full publication date if available
- Authors
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Samarth Hegde, Bruno Giotti, Brian Y. Soong, László Halász, Jessica Le Bérichel, Assaf Magen, Benoit Kloeckner, Raphaël Mattiuz, Matthew D. Park, Adam Marks, Meriem Belabed, Pauline Hamon, Theodore Chin, Leanna Troncoso, Juliana J. Lee, Dughan Ahimovic, Michael J. Bale, Grace Chung, Darwin D’souza, Krista Angeliadis, Travis Dawson, Seunghee Kim‐Schulze, Raja M. Flores, Andrew Kaufman, Florent Ginhoux, Steven Z. Josefowicz, Sai Ma, Alexander M. Tsankov, Thomas U. Marron, Brian D. Brown, Miriam MéradList of authors in order
- Landing page
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https://doi.org/10.1101/2024.06.24.600383Publisher landing page
- Open access
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YesWhether a free full text is available
- OA status
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greenOpen access status per OpenAlex
- OA URL
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https://doi.org/10.1101/2024.06.24.600383Direct OA link when available
- Concepts
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Myeloid cells, Myeloid, Progenitor, Cancer research, Progenitor cell, Immune dysregulation, Immunology, Medicine, Biology, Cell biology, Stem cell, Immune systemTop concepts (fields/topics) attached by OpenAlex
- Cited by
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6Total citation count in OpenAlex
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2025: 6Per-year citation counts (last 5 years)
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105Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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