Autophagy in natural and therapy-driven anticancer immunosurveillance

Federico Pietrocola, José Manuel Bravo-San Pedro, Lorenzo Galluzzi, Guido Kroemer

    Research output: Contribution to journalReview articlepeer-review

    55 Citations (Scopus)

    Abstract

    Autophagy is primordial for the maintenance of metabolic and genetic homeostasis in all eukaryotic organisms. Owing to its cell-intrinsic effects, autophagy robustly inhibits malignant transformation, yet can support the progression of established neoplasms as well as their resistance to conventional treatments. The notion that autophagy inhibition sensitizes neoplastic cells to chemotherapy and radiation therapy rivals with the capacity of autophagy to contribute to natural and therapy-driven anticancer immunosurveillance via a multitude of mechanisms. Indeed, autophagy ensures an optimal release of immunostimulatory signals by dying cancer cells and hence boosts their capacity to initiate an immune response. Moreover, autophagy is important for the activity of several components of the immune system involved in tumor recognition and elimination, including antigen-presenting cells and CD8 + cytotoxic T lymphocytes. In this review, we discuss how cancer cells disable autophagy to bypass immune control and how strategies aiming to enhance autophagy can be envisaged to improve the efficacy of immunogenic cancer therapies.

    Original languageEnglish
    Pages (from-to)2163-2170
    Number of pages8
    JournalAutophagy
    Volume13
    Issue number12
    DOIs
    Publication statusPublished - 2 Dec 2017

    Keywords

    • ATP
    • CD4 CD25 FOXP3 regulatory T cells
    • checkpoint blockers
    • dendritic cells
    • immunogenic cell death
    • natural killer cells

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