Interleukin-1 and neuronal injury
By S. Allan, P. Tyrrell, N. Rothwell. Nature reviews. Immunology, 2005
1,025 citations recorded by the source corpus.
Subfields: Critical Care and Intensive Care Medicine, Immunology, Neurology
View Paper: https://www.semanticscholar.org/paper/1bf5218a9e2239b60603a9fc3ad8f139b795171b
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
In Neurology
Citations in the corpus
- Regulation of innate immune responses in the brain (2009, background): “Numerous data support both a neuroprotective and a neurodestructive role for this response and have been reviewed extensivel”
- Inflammation after Intracerebral Hemorrhage (2007, background): “Interleukin-1 has gained much more attention than TNFa as a therapeutic target for stroke (Allan et al, 2005) because it has a minor role in normal brain function, and its blockade is unlikely to be associated with substantial adverse effects.”
- Inflammasomes in neuroinflammatory and neurodegenerative diseases (2019, background): “…and the central nervous system IL-1b and IL-18 have important functions in the CNS, and many cell types in the brain express their cognate receptors that initiate inflammatory signaling cascades that may contribute to neuronal injury and cell death (Allan et al, 2005; Alboni et al, 2010).”
- Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, neutral): “Brain injury produces neuroinflammation and elevated levels of brain IL-1, concomitantly with disturbances in learning and memory (Allan et al., 2005).”
- Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention. (2012, neutral): “to bind to IL-1RI without initiating signal transduction (Allan et al., 2005).”
- Inflammatory Cytokines in Experimental and Human Stroke (2012, background): “Besides IL-1RII, both soluble receptors, sIL-1RI and sIL-1RII, act as decoy receptors (Allan et al, 2005; Fogal and Hewett, 2008).”
- The role of inflammation in epilepsy (2010, neutral): “33 The activation of innate immunity and the transition to adaptive immunity are mediated by a large variety of inflammatory mediators, among which cytokines—polypeptides that act as soluble mediators of inflammation—have a pivotal role.”
- Innate and adaptive immunity during epileptogenesis and spontaneous seizures: evidence from experimental models and human temporal lobe epilepsy. (2008, background): “…and may contribute to neuronal cell loss, astrogliosis and BBB damage (Vezzani et al., 1999; De Simoni et al., 2000; Vezzani et al., 2000, 2002; Allan et al., 2005; Balosso et al., 2005; Dubé et al., 2005; Heida and Pittman, 2005; Oby and Janigro, 2006; Ravizza et al., 2006b; Vezzani and…”
- The P2X7 Receptor: A Key Player in IL-1 Processing and Release1 (2006, background): “Furthermore, it enhances expression of adhesion molecules on endothelial cells, promotes extravasation of leukocytes, modulates muscle metabolism, and induces fever (2, 13).”
- Long-term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid β-42 and α-Synuclein in Children and Young Adults (2008, background): “2001); and (3) clinical studies in children in these cities have shown healthy children with no evidence of air-pollution–associated pathology (CalderónGarcidueñas et al.”