Type I interferon inhibits interleukin-1 production and inflammasome activation.

By Greta Guarda, M. Braun, Francesco Staehli, Aubry Tardivel, C. Mattmann, I. Förster, Matthias Farlik, T. Decker, R. D. Du Pasquier, P. Romero and 1 more. Immunity, 2011

952 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/8a66e55dfd1b26ed4860e3fd0b26e8107714da4d

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Citations in the corpus

Autophagy in inflammation, infection, and immunometabolism (2021, background): “In bacterial infections however, the antimicrobial effects are attributable to autophagy whereas type I IFN activation may be an epiphenomenon that is neutral or with immunological consequence by suppressing inflammasome-driven inflammation (Burke et al., 2020; Guarda et al., 2011; Labzin et al., 20”
Dopamine controls systemic inflammation through inhibition of NLRP3 inflammasome. (2015, positive): “Type I interferon has been shown to attenuate NLRP3 inflammasome activation via Stat1-dependent manner, while nitric oxide has been identified as another negative regulator of NLRP3 inflammasome activation (Guarda et al., 2011; Mishra et al., 2013).”
Multiple early factors anticipate post-acute COVID-19 sequelae (2022, positive): “IFN-a 2 inhibition may also upregulate pro-inﬂammatory cytokines (Guarda et al., 2011), promoting ANA generation against self-antigens from tissue damage (Smatti et al., 2019).”
Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation. (2013, background): “Type I interferon has been shown to block NLRP3 inflammasome activation via Stat1-dependent manner, suggesting that success of IFN-b treatment for multiple sclerosis might indeed rely on suppressing inflammasome-mediated inflammation (Guarda et al., 2011).”
The inflammasome: an integrated view (2011, background): “IL-10-dependent suppression of proIL-1 levels is even more prominent when cells are pretreated with exogenous type I interferon (IFN), which is known to synergize with LPS to enhance IL-10 production (16, 44).”
Into the Eye of the Cytokine Storm (2012, background): “Inflammasomes are cytosolic macromolecular complexes comprised of members of the nucleotidebinding domain and leucine-rich-repeat-containing receptor (NLR) family (the NLRP3 inflammasome is one the best characterized) that produce IL-1 and IL-18 in defense against pathogens, and their activity is re”
Repurposing mitochondria from ATP production to ROS generation drives a pro-inflammatory phenotype in macrophages that depends on succinate oxidation by complex II (2016, background): “Type I IFNs are also of interest, as they inhibit LPS-induced proIL-1b production and boost IL-10 in BMDMs (Guarda et al., 2011), providing further mechanistic evidence for the regulation of IL-10, and indeed of IL-1b, by these agents.”
Inflammasomes in health and disease (2012, background): “Examples of these signals are type I interferons or interactions between CD4 p T cells and macrophages or dendritic cells, respectively, leading to transcriptional and post-transcriptional downregulation of inflammasome activit”
TRIF Licenses Caspase-11-Dependent NLRP3 Inflammasome Activation by Gram-Negative Bacteria (2012, positive): “Type I IFN has been shown to impair transcription of pro-IL-1b, thereby reducing the pool of precursor levels (Guarda et al., 2011).”