IFN-Independent STING Signaling: Friend or Foe?

Volker Böhnert; Christopher Ritchie; Lingyin Li

doi:10.1016/j.immuni.2020.06.021

IFN-Independent STING Signaling: Friend or Foe?

Immunity. 2020 Jul 14;53(1):8-10. doi: 10.1016/j.immuni.2020.06.021.

Authors

Volker Böhnert¹, Christopher Ritchie¹, Lingyin Li²

Affiliations

¹ Department of Biochemistry, Stanford University, Stanford, CA 94305, USA; Institute of Chemistry, Engineering, and Medicine for Human Health (ChEM-H), Stanford University, Stanford, CA 94305, USA.
² Department of Biochemistry, Stanford University, Stanford, CA 94305, USA; Institute of Chemistry, Engineering, and Medicine for Human Health (ChEM-H), Stanford University, Stanford, CA 94305, USA. Electronic address: lingyinl@stanford.edu.

PMID: 32668231
DOI: 10.1016/j.immuni.2020.06.021

Abstract

In this issue, Wu et al. demonstrate the importance of the neglected interferon (IFN)-independent STING signaling axis in mice. They find that although this axis is important for antiviral HSV-1 resistance, it has a pro-cancer role by promoting T cell death.

Publication types

Comment

MeSH terms

Animals
Antiviral Agents
Bites and Stings*
Interferons*
Membrane Proteins / genetics
Mice
Tumor Escape

Substances

Antiviral Agents
Membrane Proteins
Interferons