de.mpg.escidoc.pubman.appbase.FacesBean
English
 
Help Guide Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Oxeiptosis, a ROS-induced caspase-independent apoptosis-like cell-death pathway

MPS-Authors
http://pubman.mpdl.mpg.de/cone/persons/resource/persons78126

Holze,  Cathleen
Pichlmair, Andreas / Innate Immunity, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons185890

Haas,  Darya A.
Pichlmair, Andreas / Innate Immunity, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons77736

Benda,  Christian
Conti, Elena / Structural Cell Biology, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons127956

Hubel,  Philipp
Pichlmair, Andreas / Innate Immunity, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons214253

Pennemann,  Friederike L.
Pichlmair, Andreas / Innate Immunity, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78510

Pichlmair,  Andreas
Pichlmair, Andreas / Innate Immunity, Max Planck Institute of Biochemistry, Max Planck Society;

Fulltext (public)
There are no public fulltexts available
Supplementary Material (public)
There is no public supplementary material available
Citation

Holze, C., Michaudel, C., Mackowiak, C., Haas, D. A., Benda, C., Hubel, P., et al. (2018). Oxeiptosis, a ROS-induced caspase-independent apoptosis-like cell-death pathway. Nature Immunology, 19, 130-140. doi:10.1038/s41590-017-0013-y.


Cite as: http://hdl.handle.net/21.11116/0000-0000-2F6E-2
Abstract
Reactive oxygen species (ROS) are generated by virus-infected cells; however, the physiological importance of ROS generated under these conditions is unclear. Here we found that the inflammation and cell death induced by exposure of mice or cells to sources of ROS were not altered in the absence of canonical ROS-sensing pathways or known cell-death pathways. ROS-induced cell-death signaling involved interactions among the cellular ROS sensor and antioxidant factor KEAP1, the phosphatase PGAM5 and the proapoptotic factor AIFM1. Pgam5–/– mice showed exacerbated lung inflammation and proinflammatory cytokines in an ozone-exposure model. Similarly, challenge with influenza A virus led to increased infiltration of the virus, lymphocytic bronchiolitis and reduced survival of Pgam5–/– mice. This pathway, which we have called ‘oxeiptosis’, was a ROS-sensitive, caspase independent, non-inflammatory cell-death pathway and was important for protection against inflammation induced by ROS or ROS-generating agents such as viral pathogens.