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Holze, C.* ; Michaudel, C.* ; Mackowiak, C.* ; Haas, D.A.* ; Benda, C.* ; Hubel, P.* ; Pennemann, F.L.* ; Schnepf, D.* ; Wettmarshausen, J. ; Braun, M.* ; Leung, D.W.* ; Amarasinghe, G.K.* ; Perocchi, F. ; Staeheli, P.* ; Ryffel, B.* ; Pichlmair, A.*

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

Nat. Immunol. 19, 1-11 (2017)
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Oxidative Stress; Nadph Oxidase; Molecular-mechanisms; Hydrogen-peroxide; Virus; Keap1; Protein; Necroptosis; Activation; Nrf2
ISSN (print) / ISBN 1529-2908
e-ISSN 1529-2916
Zeitschrift Nature Immunology
Quellenangaben Band: 19, Heft: 2, Seiten: 1-11 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Verlagsort New York
Begutachtungsstatus Peer reviewed