Reprogramming of tumor-associated macrophages with anticancer therapies: Radiotherapy versus chemo- and immunotherapies

Résultats de recherche: Contribution à un journal/une revueArticle

Résumé

Tumor-associated macrophages (TAMs) play a central role in tumor progression, metastasis, and recurrence after treatment. Macrophage plasticity and diversity allow their classification along a M1-M2 polarization axis. Tumor-associated macrophages usually display a M2-like phenotype, associated with pro-tumoral features whereas M1 macrophages exert antitumor functions. Targeting the reprogramming of TAMs toward M1-like macrophages would thus be an efficient way to promote tumor regression. This can be achieved through therapies including chemotherapy, immunotherapy, and radiotherapy (RT). In this review, we first describe how chemo- and immunotherapies can target TAMs and, second, we detail how RT modifies macrophage phenotype and present the molecular pathways that may be involved. The identification of irradiation dose inducing macrophage reprogramming and of the underlying mechanisms could lead to the design of novel therapeutic strategies and improve synergy in combined treatments.

langueAnglais
Numéro d'article828
Nombre de pages19
journalFrontiers in Immunology
Volume8
NuméroJUL
Les DOIs
étatPublié - 2017

Empreinte digitale

Immunotherapy
Radiotherapy
Macrophages
Drug Therapy
Neoplasms
Therapeutics
Phenotype
Neoplasm Metastasis
Recurrence

mots-clés

    Citer ceci

    @article{db16e6aa1f4446ea9336db378a5eead0,
    title = "Reprogramming of tumor-associated macrophages with anticancer therapies: Radiotherapy versus chemo- and immunotherapies",
    abstract = "Tumor-associated macrophages (TAMs) play a central role in tumor progression, metastasis, and recurrence after treatment. Macrophage plasticity and diversity allow their classification along a M1-M2 polarization axis. Tumor-associated macrophages usually display a M2-like phenotype, associated with pro-tumoral features whereas M1 macrophages exert antitumor functions. Targeting the reprogramming of TAMs toward M1-like macrophages would thus be an efficient way to promote tumor regression. This can be achieved through therapies including chemotherapy, immunotherapy, and radiotherapy (RT). In this review, we first describe how chemo- and immunotherapies can target TAMs and, second, we detail how RT modifies macrophage phenotype and present the molecular pathways that may be involved. The identification of irradiation dose inducing macrophage reprogramming and of the underlying mechanisms could lead to the design of novel therapeutic strategies and improve synergy in combined treatments.",
    keywords = "Chemotherapy, Nuclear factor kappa B, Polarization immunotherapy, Radiotherapy, Reactive oxygen species, Reprogramming, Tumor-associated macrophages",
    author = "G\{'e}raldine Genard and St\{'e}phane Lucas and Carine Michiels",
    year = "2017",
    doi = "10.3389/fimmu.2017.00828",
    language = "English",
    volume = "8",
    journal = "Frontiers in Immunology",
    issn = "1664-3224",
    publisher = "Frontiers Research Foundation",
    number = "JUL",

    }

    TY - JOUR

    T1 - Reprogramming of tumor-associated macrophages with anticancer therapies

    T2 - Frontiers in Immunology

    AU - Genard,Géraldine

    AU - Lucas,Stéphane

    AU - Michiels,Carine

    PY - 2017

    Y1 - 2017

    N2 - Tumor-associated macrophages (TAMs) play a central role in tumor progression, metastasis, and recurrence after treatment. Macrophage plasticity and diversity allow their classification along a M1-M2 polarization axis. Tumor-associated macrophages usually display a M2-like phenotype, associated with pro-tumoral features whereas M1 macrophages exert antitumor functions. Targeting the reprogramming of TAMs toward M1-like macrophages would thus be an efficient way to promote tumor regression. This can be achieved through therapies including chemotherapy, immunotherapy, and radiotherapy (RT). In this review, we first describe how chemo- and immunotherapies can target TAMs and, second, we detail how RT modifies macrophage phenotype and present the molecular pathways that may be involved. The identification of irradiation dose inducing macrophage reprogramming and of the underlying mechanisms could lead to the design of novel therapeutic strategies and improve synergy in combined treatments.

    AB - Tumor-associated macrophages (TAMs) play a central role in tumor progression, metastasis, and recurrence after treatment. Macrophage plasticity and diversity allow their classification along a M1-M2 polarization axis. Tumor-associated macrophages usually display a M2-like phenotype, associated with pro-tumoral features whereas M1 macrophages exert antitumor functions. Targeting the reprogramming of TAMs toward M1-like macrophages would thus be an efficient way to promote tumor regression. This can be achieved through therapies including chemotherapy, immunotherapy, and radiotherapy (RT). In this review, we first describe how chemo- and immunotherapies can target TAMs and, second, we detail how RT modifies macrophage phenotype and present the molecular pathways that may be involved. The identification of irradiation dose inducing macrophage reprogramming and of the underlying mechanisms could lead to the design of novel therapeutic strategies and improve synergy in combined treatments.

    KW - Chemotherapy

    KW - Nuclear factor kappa B

    KW - Polarization immunotherapy

    KW - Radiotherapy

    KW - Reactive oxygen species

    KW - Reprogramming

    KW - Tumor-associated macrophages

    UR - http://www.scopus.com/inward/record.url?scp=85023165096&partnerID=8YFLogxK

    U2 - 10.3389/fimmu.2017.00828

    DO - 10.3389/fimmu.2017.00828

    M3 - Article

    VL - 8

    JO - Frontiers in Immunology

    JF - Frontiers in Immunology

    SN - 1664-3224

    IS - JUL

    M1 - 828

    ER -