Silence of the ROS

Judith Agudo; Brian D Brown

doi:10.1016/j.immuni.2016.02.027

Silence of the ROS

Immunity. 2016 Mar 15;44(3):520-522. doi: 10.1016/j.immuni.2016.02.027.

Authors

Judith Agudo¹, Brian D Brown²

Affiliations

¹ Genetics and Genomic Sciences Department, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
² Genetics and Genomic Sciences Department, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address: brian.brown@mssm.edu.

PMID: 26982360
DOI: 10.1016/j.immuni.2016.02.027

Abstract

Reactive oxygen species (ROS) are generated during T cell activation and serve a signaling function but can also be damaging. In this issue of Immunity, Zhang et al. (2016) show that miR-23a prevents ROS-elicited necrosis by suppressing cyclophilin D (PPIF), a regulator of ROS escape from mitochondria.

Publication types

Comment

MeSH terms

Animals
CD4-Positive T-Lymphocytes / immunology*
Listeria monocytogenes / immunology*
Listeriosis / immunology*
Liver / pathology*
MicroRNAs / metabolism*
Mitochondria / metabolism*

Substances

MicroRNAs