Data from Matrix-Targeting Immunotherapy Controls Tumor Growth and Spread by Switching Macrophage Phenotype Article Swipe

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Claire Deligne , Devadarssen Murdamoothoo , Anís N. Gammage , Martha Gschwandtner , William Erne , Thomas Loustau , Anna M. Marzeda , Raphaël Carapito , Nicodème Paul , Inés Velázquez-Quesada , Imogen Mazzier , Zhen Sun , Gertraud Orend , Kim S. Midwood ·

YOU? · · 2023 · Open Access · · DOI: https://doi.org/10.1158/2326-6066.c.6550338.v1

The interplay between cancer cells and immune cells is a key determinant of tumor survival. Here, we uncovered how tumors exploit the immunomodulatory properties of the extracellular matrix to create a microenvironment that enables their escape from immune surveillance. Using orthotopic grafting of mammary tumor cells in immunocompetent mice and autochthonous models of breast cancer, we discovered how tenascin-C, a matrix molecule absent from most healthy adult tissues but expressed at high levels and associated with poor patient prognosis in many solid cancers, controls the immune status of the tumor microenvironment. We found that, although host-derived tenascin-C promoted immunity via recruitment of proinflammatory, antitumoral macrophages, tumor-derived tenascin-C subverted host defense by polarizing tumor-associated macrophages toward a pathogenic, immune-suppressive phenotype. Therapeutic monoclonal antibodies that blocked tenascin-C activation of Toll-like receptor 4 reversed this phenotypic switch in vitro and reduced tumor growth and lung metastasis in vivo, providing enhanced benefit in combination with anti–PD-L1 over either treatment alone. Combined tenascin-C:macrophage gene-expression signatures delineated a significant survival benefit in people with breast cancer. These data revealed a new approach to targeting tumor-specific macrophage polarization that may be effective in controlling the growth and spread of breast tumors.

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Tenascin C Tumor microenvironment Immune system Cancer research Macrophage polarization Tenascin Biology Macrophage Immunology Mammary tumor Immunotherapy Metastasis Extracellular matrix M2 Macrophage Breast cancer Cancer Cell biology In vitro Fibronectin Genetics Biochemistry

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Type: preprint
Language: en
Landing Page: https://doi.org/10.1158/2326-6066.c.6550338.v1
OA Status: gold
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DOI: https://doi.org/10.1158/2326-6066.c.6550338.v1

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Title: Data from Matrix-Targeting Immunotherapy Controls Tumor Growth and Spread by Switching Macrophage Phenotype

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Type: preprint

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Language: en

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Publication year: 2023

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Publication date: 2023-04-04

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Authors: Claire Deligne, Devadarssen Murdamoothoo, Anís N. Gammage, Martha Gschwandtner, William Erne, Thomas Loustau, Anna M. Marzeda, Raphaël Carapito, Nicodème Paul, Inés Velázquez-Quesada, Imogen Mazzier, Zhen Sun, Gertraud Orend, Kim S. Midwood

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Landing page: https://doi.org/10.1158/2326-6066.c.6550338.v1

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Concepts: Tenascin C, Tumor microenvironment, Immune system, Cancer research, Macrophage polarization, Tenascin, Biology, Macrophage, Immunology, Mammary tumor, Immunotherapy, Metastasis, Extracellular matrix, M2 Macrophage, Breast cancer, Cancer, Cell biology, In vitro, Fibronectin, Genetics, Biochemistry

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abstract_inverted_index.tumors.</p></div>	193
abstract_inverted_index.<div>Abstract<p>The	0
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