Journal article
Type-I interferon signaling through ISGF3 complex is required for sustained Rip3 activation and necroptosis in macrophages
Abstract
Myeloid cells play a critical role in perpetuating inflammation during various chronic diseases. Recently the death of macrophages through programmed necrosis (necroptosis) has emerged as an important mechanism in inflammation and pathology. We evaluated the mechanisms that lead to the induction of necrotic cell death in macrophages. Our results indicate that type I IFN (IFN-I) signaling is a predominant mechanism of necroptosis, because …
Authors
McComb S; Cessford E; Alturki NA; Joseph J; Shutinoski B; Startek JB; Gamero AM; Mossman KL; Sad S
Journal
Proceedings of the National Academy of Sciences of the United States of America, Vol. 111, No. 31, pp. e3206–e3213
Publisher
Proceedings of the National Academy of Sciences
Publication Date
August 5, 2014
DOI
10.1073/pnas.1407068111
ISSN
0027-8424
Associated Experts
Fields of Research (FoR)
Medical Subject Headings (MeSH)
AnimalsApoptosisEnzyme ActivationInflammationInterferon Type IInterferon-Stimulated Gene Factor 3, gamma SubunitLipopolysaccharidesMacrophagesMiceMice, Inbred C57BLModels, BiologicalNecrosisOligopeptidesPoly I-CReceptor, Interferon alpha-betaReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionTumor Necrosis Factor-alpha