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Involvement of the M-CSF/IL-34/CSF-1R pathway in malignant pleural mesothelioma

Thibaut Blondy1, Sènan Mickael d'Almeida2,3,4, Tina Briolay1

  • 1Université de Nantes, CNRS, INSERM, CRCINA, F-44000 Nantes, France.

Journal for Immunotherapy of Cancer
|June 26, 2020
PubMed
Abstract

Insights

The M-CSF/IL-34/CSF-1R pathway drives immunosuppressive macrophage formation in malignant pleural mesothelioma (MPM). Targeting this pathway may enhance immunotherapies for asbestos-related cancer.

Area of Science:

  • Oncology
  • Immunology
  • Cell Biology

Background:

  • Malignant pleural mesothelioma (MPM) is a rare, aggressive cancer linked to asbestos exposure.
  • The tumor microenvironment, especially macrophages, is critical in MPM development.
  • The M-CSF (CSF-1)/IL-34/CSF-1R pathway's role in MPM macrophage formation requires investigation.

Purpose of the Study:

  • To investigate the involvement of the M-CSF/IL-34/CSF-1R pathway in macrophage formation in MPM.
  • To correlate cytokine expression with patient survival and tumor characteristics.
  • To assess the pathway's impact on the tumor immune microenvironment and T cell function.

Main Methods:

  • Analysis of patient-derived pleural effusions, tumors, and cell lines.
  • Cytokine expression analysis via real-time PCR and ELISA.
  • Utilized The Cancer Genome Atlas and a 3D coculture model with MPM cells, monocytes, and CD8+ T cells.

Main Results:

  • High IL-34 levels in pleural effusions correlated with shorter patient survival.
  • Tumor CSF1 expression linked to M2-like macrophage markers, while IL34 expression showed distinct correlations.
  • MPM cells, particularly those with CDKN2A alterations, express high IL34 and promote immunosuppressive macrophages via CSF-1R, inhibiting CD8+ T cell cytotoxicity.

Conclusions:

  • The M-CSF/IL-34/CSF-1R pathway is significantly involved in MPM pathogenesis.
  • This pathway contributes to immune suppression within the MPM tumor microenvironment.
  • Targeting the M-CSF/IL-34/CSF-1R pathway presents a potential therapeutic strategy for MPM, enhancing immunotherapeutic efficacy.
Keywords:
immunologyoncologytumors

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