STING controls T cell memory fitness during infection through T cell-intrinsic and IDO-dependent mechanisms

Proc Natl Acad Sci U S A. 2023 Jan 17;120(3):e2205049120. doi: 10.1073/pnas.2205049120. Epub 2023 Jan 12.

Abstract

Stimulator of interferon genes (STING) signaling has been extensively studied in inflammatory diseases and cancer, while its role in T cell responses to infection is unclear. Using Listeria monocytogenes strains engineered to induce different levels of c-di-AMP, we found that high STING signals impaired T cell memory upon infection via increased Bim levels and apoptosis. Unexpectedly, reduction of TCR signal strength or T cell-STING expression decreased Bim expression, T cell apoptosis, and recovered T cell memory. We found that TCR signal intensity coupled STING signal strength to the unfolded protein response (UPR) and T cell survival. Under strong STING signaling, Indoleamine-pyrrole 2,3-dioxygenase (IDO) inhibition also reduced apoptosis and led to a recovery of T cell memory in STING sufficient CD8 T cells. Thus, STING signaling regulates CD8 T cell memory fitness through both cell-intrinsic and extrinsic mechanisms. These studies provide insight into how IDO and STING therapies could improve long-term T cell protective immunity.

Keywords: CD8 T cell memory; STING; TCR.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD8-Positive T-Lymphocytes
  • Indoleamine-Pyrrole 2,3,-Dioxygenase / metabolism
  • Memory T Cells
  • Receptors, Antigen, T-Cell* / genetics
  • Signal Transduction*

Substances

  • Receptors, Antigen, T-Cell
  • Indoleamine-Pyrrole 2,3,-Dioxygenase