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Details on Person Diverse molecules of host-cell origin may serve as endogenou...

Class:IdSummation:5686933
_displayNameDiverse molecules of host-cell origin may serve as endogenou...
_timestamp2023-01-22 05:46:22
created[InstanceEdit:5686931] Shamovsky, Veronica, 2015-04-06
literatureReference[LiteratureReference:5686936] Endogenous ligands of TLR2 and TLR4: agonists or assistants?
[LiteratureReference:5686934] DAMPening inflammation by modulating TLR signalling
[LiteratureReference:6804082] Citrullination enhances the pro-inflammatory response to fibrin in rheumatoid arthritis synovial fibroblasts
[LiteratureReference:6804062] Immune complexes containing citrullinated fibrinogen costimulate macrophages via Toll-like receptor 4 and Fcγ receptor
[LiteratureReference:6804081] Citrullination of histone H3 interferes with HP1-mediated transcriptional repression
[LiteratureReference:6804066] Peptidylarginine deiminase 4 and citrullination in health and disease
modified[InstanceEdit:6793748] Shamovsky, Veronica, 2015-09-04
[InstanceEdit:6804073] Shamovsky, Veronica, 2015-10-08
[InstanceEdit:6804112] Shamovsky, Veronica, 2015-10-08
[InstanceEdit:6805948] Shamovsky, Veronica, 2015-10-21
[InstanceEdit:9824672] Shamovsky, Veronica, 2023-01-22
textDiverse molecules of host-cell origin may serve as endogenous ligands of Toll-like receptors (TLRs) (Erridge C 2010; Piccinini AM & Midwood KS 2010). These molecules are known as damage-associated molecular patterns (DAMPs). DAMPs are immunologically silent in healthy tissues but become active upon tissue damage during both infectious and sterile insult. DAMPs are released from necrotic cells or secreted from activated cells in response to tissue damage to mediate tissue repair by promoting inflammatory responses. However, DAMPs have also been implicated in the pathogenesis of many inflammatory and autoimmune diseases, including rheumatoid arthritis (RA), cancer, and atherosclerosis. The mechanism underlying the switch from DAMPs that initiate controlled tissue repair, to those that mediate chronic, uncontrolled inflammation is still unclear. Recent evidence suggests that an abnormal increase in protein citrullination is involved in disease pathophysiology (Anzilotti C et al. 2010; Sanchez-Pernaute O et al. 2013; Sokolove J et al. 2011; Sharma P et al. 2012). Citrullination is a post-translational modification event mediated by peptidyl-arginine deaminase enzymes which catalyze the deimination of proteins by converting arginine residues into citrullines in the presence of calcium ions.
(summation)[Pathway:5686938] Regulation of TLR by endogenous ligand [Homo sapiens]
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