Cutting Edge: Activation of STING in T Cells Induces Type I IFN Responses and Cell Death

J Immunol. 2017 Jul 15;199(2):397-402. doi: 10.4049/jimmunol.1601999. Epub 2017 Jun 14.

Abstract

Stimulator of interferon genes (STING) was initially described as a sensor of intracellular bacterial and viral DNA and a promising adjuvant target in innate immune cells; more recently STING has also been shown to detect endogenous DNA and play a role in tumor immunity and autoimmune disease development. Thus far STING has been studied in macrophages and dendritic cells. In this study, to our knowledge we provide the first evidence of STING activation in T cells, in which STING agonists not only provoke type I IFN production and IFN-stimulated gene expression, mirroring the response of innate cells, but are also capable of activating cell stress and death pathways. Our results suggest a re-evaluation of STING agonist-based therapies may be necessary to identify the possible effects on the T cell compartment. Conversely, the effects of STING on T cells could potentially be harnessed for therapeutic applications.

MeSH terms

  • Animals
  • Cell Death*
  • Endoplasmic Reticulum Stress
  • Immunity, Innate
  • Interferon Type I / biosynthesis*
  • Interferon Type I / immunology*
  • Lymphocyte Activation
  • Macrophages / immunology
  • Macrophages / metabolism
  • Membrane Proteins / deficiency
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Mice
  • Sequence Analysis, RNA
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism
  • T-Lymphocytes / physiology

Substances

  • Interferon Type I
  • Membrane Proteins
  • Sting1 protein, mouse