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• W2000856450 abstract "Type I interferons (IFNs) are pleiotropic cytokines that have been implicated in the pathogenesis of systemic lupus erythematosus (SLE). A key aspect of type I IFN biology is that previous exposure to type I IFNs alters subsequent cellular responses to extracellular stimuli. Type I IFNs may either prime cells for stronger responses to viruses, bacterial pathogens and cytokines such as IL-6 and IFN-gamma, or may suppress cellular responses to LPS and TNFalpha. Herein, we review type I IFN signal transduction via the Jak-STAT pathway, and mechanisms by which type I IFNs prime or suppress responses to environmental factors. We develop a hypothesis that type I IFN-dependent priming/enhancement of cellular responses to pro-inflammatory cytokines such as IFNgamma and IL-6 contributes to pathogenesis of SLE. In addition, cross-regulation between type I IFNs and TNFalpha and its potential role in SLE pathogenesis is discussed." @default.
• W2000856450 created "2016-06-24" @default.
• W2000856450 creator A5087516945 @default.
• W2000856450 date "2003-12-01" @default.
• W2000856450 modified "2023-10-05" @default.
• W2000856450 title "Type I Interferon Modulation of Cellular Responses to Cytokines and Infectious Pathogens: Potential Role in SLE Pathogenesis" @default.
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• W2000856450 doi "https://doi.org/10.1080/08916930310001605882" @default.
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