Immunological and inflammatory functions of the interleukin-1 family.
By C. A. Dinarello. Annual Review of Immunology, 2009
3,567 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/b15b1d56336617bbeb383cf0d73fd6da2512e07f
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Citations in the corpus
- IL-1 receptor antagonist ameliorates inflammasome-dependent alcoholic steatohepatitis in mice. (2012, background): “Although Casp-1 cleaves IL-1β, IL-18, and IL-33 (8), and IL-1R1 recognizes IL-1α, IL-1β, and IL-1Ra (16), our study provides several lines of evidence that IL-1β — not IL-18, IL-33, or IL-1α — is the primary cytokine that mediates the pathogenic effects of activated inflammasome in ALD.”
- Canonical Nlrp3 inflammasome links systemic low grade inflammation to functional decline in aging (2013, neutral): “Depending on the disease model, several redundant upstream mechanisms control the processing and secretion of mature IL-1b; these include neutrophil-derived serine proteinase 3 and granzyme A (Dinarello, 2009).”
- The sterile inflammatory response (2010, background): “IL-1β is a potent multifunctional proinflammatory cytokine, whose activity is controlled at the transcriptional, translational, maturation and secretion levels (64).”
- Mechanisms and functions of inflammasomes. (2014, background): “IL-18 is important for IL-17 expression by Th17 cells and may polarize T cells toward Th1 or Th2 profiles in combination with other cytokines (Dinarello, 2009).”
- Interleukin-1 (IL-1) Pathway (2010, background): “The occurrence of severe multiorgan inflammation in patients with homozygous mutations or deletions of the gene encoding interleukin-1 receptor antagonist (IL-1RA) (7, 8) and the successful blockade of inflammatory reactions in humans by application of recombinant IL-1RA (5) or antibodies to IL-1β (”
- Redox Regulation of NLRP3 Inflammasomes: ROS as Trigger or Effector? (2015, neutral): “As mentioned earlier, these mechanisms may potentially include other downstream targets of caspase-1 independent of IL-1 b or IL-18, such as pyroptosis, inhibition of glycolysis, noninflammatory cell death, and activation of lipid biogenesis pathways (49, 65, 90, 115).”
- The Role of Markers of Inflammation in Traumatic Brain Injury (2013, background): “The IL-1 family includes the closely related agonists IL-1α and IL-1β, the antagonist IL-1ra, and the other family member, the agonist IL-18 (Dinarello, 1994, 1998, 2009; Barksby et al., 2007).”
- Human Monocytes Engage an Alternative Inflammasome Pathway. (2016, neutral): “…production is associated with monogenetic auto-inflammatory diseases (Masters et al., 2009), but also with ligand-dependent, multifactorial, sterile inflammatory conditions, such as atherosclerosis, type 2 diabetes, Alzheimer’s disease, or gout (Dinarello, 2009, 2011; Haneklaus and O’Neill, 2015).”
- Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis. (2012, background): “Secretion of interleukin-1b (IL-1b), a potent pyrogen that elicits a strong proinflammatory response (Dinarello, 2009), is tightly controlled by a diverse class of cytosolic complexes known as the inflammasome (Latz, 2010).”
- Rethinking IL-6 and CRP: Why they are more than inflammatory biomarkers, and why it matters. (2018, neutral): “IL-1β also prompts vasodilation, and increases expression of adhesion molecules in the endothelium, which promotes infiltration of immune cells into affected tissue (Dinarello, 2009).”
- Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes. (2014, background): “[50] Dinarello CA.”
- Cytokines and chemokines: At the crossroads of cell signalling and inflammatory disease. (2014, background): “It is also important in the secretion of acute phase proteins by the liver [48], which it does in cooperation with IL-1 [6].”
- NLRP3 Inflammasome and the IL-1 Pathway in Atherosclerosis. (2018, background): “Mature caspase-1 has a very short half-life37 and is therefore not well suited for the extracellular maturation of pro–IL-1β.”
- The NALP3/NLRP3 Inflammasome Instigates Obesity-Induced Autoinflammation and Insulin Resistance (2011, background): “The release of bioactive IL-1β and IL-18 from macrophages is in turn dependent on autocatalytic activation of procaspase-1 zymogen into enzymatically active 10-kDa and 20-kDa caspase-1 heterodimer”
- The role of inflammation in epilepsy (2010, neutral): “…mechanisms include production of proteins that compete with cytokines to bind their receptors, such as IL-1 receptor antagonist protein (IL-1ra), 41 and decoy receptors that bind cytokines and chemokines but are incapable of signaling, thereby acting as molecular traps to prevent such ligands…”