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- W2016430217 startingPage "41" @default.
- W2016430217 abstract "Summary: Activated macrophages and their inflammatory products play a key role in innate immunity and in pathogenesis of autoimmune/inflammatory diseases. Macrophage activation needs to be tightly regulated to rapidly mount responses to infectious challenges but to avoid toxicity associated with excessive activation. Rapid and potent macrophage activation is driven by cytokine‐mediated feedforward loops, while excessive activation is prevented by feedback inhibition. Here we discuss feedforward mechanisms that augment macrophage responses to Toll‐like receptor (TLR) ligands and cytokines that are mediated by signal transducer and activator of transcription 1 (STAT1) and induced by interferon‐γ (IFN‐γ). IFN‐γ also drives full macrophage activation by inactivating feedback inhibitory mechanisms, such as those mediated by interleukin‐10 (IL‐10), and STAT3. Priming of macrophages with IFN‐γ reprograms cellular responses to other cytokines, such as type I IFNs and IL‐10, with a shift toward pro‐inflammatory STAT1‐dominated responses. Similar but partially distinct priming effects are induced by other cytokines that activate STAT1, including type I IFNs and IL‐27. We propose a model whereby opposing feedforward and feedback inhibition loops crossregulate each other to fine tune macrophage activation. In addition, we discuss how dysregulation of the balance between feedforward and feedback inhibitory mechanisms can contribute to the pathogenesis of autoimmune and inflammatory diseases, such as rheumatoid arthritis and systemic lupus erythematosus." @default.
- W2016430217 created "2016-06-24" @default.
- W2016430217 creator A5065731483 @default.
- W2016430217 creator A5072083932 @default.
- W2016430217 creator A5087516945 @default.
- W2016430217 date "2008-10-30" @default.
- W2016430217 modified "2023-10-12" @default.
- W2016430217 title "Regulation of interferon and Toll-like receptor signaling during macrophage activation by opposing feedforward and feedback inhibition mechanisms" @default.
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