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Macrophage-Targeted Therapy Unlocks Antitumoral Cross-talk between IFNγ-Secreting Lymphocytes and IL12-Producing Dendritic Cells
Journal article   Open access   Peer reviewed

Macrophage-Targeted Therapy Unlocks Antitumoral Cross-talk between IFNγ-Secreting Lymphocytes and IL12-Producing Dendritic Cells

Christina Pfirschke, Rapolas Zilionis, Camilla Engblom, Marius Messemaker, Angela E Zou, Steffen Rickelt, Nicolas A Gort-Freitas, Yunkang Lin, Ruben Bill, Marie Siwicki, …
Cancer immunology research, v 10(1), pp 40-55
Jan 2022
PMID: 34795032
url
https://doi.org/10.1158/2326-6066.cir-21-0326View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open
url
https://doi.org/10.1158/2326-6066.CIR-21-0326View
Published, Version of Record (VoR) Open

Abstract

Animals Benzothiazoles - pharmacology Cell Line, Tumor Dendritic Cells - immunology Female Immunotherapy - methods Interferon-gamma - metabolism Interleukin-12 - metabolism Lung Neoplasms - immunology Lung Neoplasms - therapy Mice Mice, Inbred C57BL Picolinic Acids - pharmacology Tumor Microenvironment - drug effects Tumor-Associated Macrophages - drug effects Tumor-Associated Macrophages - metabolism Xenograft Model Antitumor Assays
Macrophages often abound within tumors, express colony-stimulating factor 1 receptor (CSF1R), and are linked to adverse patient survival. Drugs blocking CSF1R signaling have been used to suppress tumor-promoting macrophage responses; however, their mechanisms of action remain incompletely understood. Here, we assessed the lung tumor immune microenvironment in mice treated with BLZ945, a prototypical small-molecule CSF1R inhibitor, using single-cell RNA sequencing and mechanistic validation approaches. We showed that tumor control was not caused by CSF1R cell depletion; instead, CSF1R targeting reshaped the CSF1R cell landscape, which unlocked cross-talk between antitumoral CSF1R cells. These cells included IFNγ-producing natural killer and T cells, and an IL12-producing dendritic cell subset, denoted as DC , which were all necessary for CSF1R inhibitor-mediated lung tumor control. These data indicate that CSF1R targeting can activate a cardinal cross-talk between cells that are not macrophages and that are essential to mediate the effects of T cell-targeted immunotherapies and promote antitumor immunity.

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Collaboration types
Industry collaboration
Domestic collaboration
International collaboration
Web of Science research areas
Immunology
Oncology
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