Autophagy in natural and therapy-driven anticancer immunosurveillance. Academic Article uri icon

Overview

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.

publication date

  • July 26, 2017

Research

keywords

  • Autophagy
  • Monitoring, Immunologic
  • Neoplasms

Identity

PubMed Central ID

  • PMC5788556

Scopus Document Identifier

  • 85041170745

Digital Object Identifier (DOI)

  • 10.1080/15548627.2017.1310356

PubMed ID

  • 28598229

Additional Document Info

volume

  • 13

issue

  • 12