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Review ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Immunol. | doi: 10.3389/fimmu.2019.02309

The metabolic profile of tumour and virally infected cells shapes their microenvironment counteracting T cell immunity

  • 1Karolinska Institute (KI), Sweden
  • 2AstraZeneca (United Kingdom), United Kingdom
  • 3Department of Medical Oncology and Hematology, Princess Margaret Cancer Centre, Canada
  • 4Department of Medicine, University of Toronto, Canada
  • 5Department of Infectious Diseases, King’s College London, United Kingdom

Upon activation naïve T cells undergo metabolic changes to form different subsets of effector or regulatory cells, and subsequently remodel their metabolic profile again to form memory. Interfering with these metabolic alterations leads to abrogation or reprogramming of T cell differentiation, demonstrating the importance of this pathway in T cell development. It has long been appreciated that the conversion of a healthy cell to a cancerous cell is accompanied by metabolic changes, which support uncontrolled proliferation. Especially in solid tumours these metabolic changes significantly influence the tumour microenvironment (TME) and affect tumour infiltrating immune cells. The TME is often hypoxic and nutrient depleted, additionally tumour cells produce co-inhibitory signals, together supressing the immune response. Interestingly, viruses can stimulate a metabolism akin to that seen in tumour cells in their host cells and even in neighbouring cells (e.g. via transfer of virally modified extracellular vesicles). Thus viruses create their own niche which favours viral persistence and propagation, while again keeping the immune response at bay.
In this review we will focus on the mechanisms employed by tumour cells and viruses influencing T cell metabolic regulation and the impact they have on shaping T cell fate.

Keywords: Metabolism, tumor, T cell, virus, hypoxia

Received: 01 Jul 2019; Accepted: 12 Sep 2019.

Copyright: © 2019 Magalhaes, Yogev, Mattsson and Schurich. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Dr. Isabelle Magalhaes, Karolinska Institute (KI), Solna, Sweden, isabelle.magalhaes@ki.se
Dr. Anna Schurich, Department of Infectious Diseases, King’s College London, London, United Kingdom, anna.schurich@kcl.ac.uk