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Endogenous toll-like receptor ligands and their biological significance.

Yu L, Wang L, Chen S - J. Cell. Mol. Med. (2010)

Bottom Line: Toll-like receptors (TLRs), a family of pattern recognition receptors, recognize and respond to conserved components of microbes and play a crucial role in both innate and adaptive immunity.Putative endogenous TLR ligands include proteins and peptides, polysaccharides and proteoglycan, nucleic acids and phospholipids, which are cellular components, particularly extracellular matrix degradation products.The ability of TLRs to recognize endogenous stimulators appears to be essential to their function in regulating non-infectious inflammation.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, the First Affiliated Hospital, Sun Yat-sen (Zhongshan) University, Guangzhou, P.R. China.

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A proposed mechanism of inflammatory response in ischemia/reperfusion injury. Ischemia/reperfusion injury results in release of endogenous TLR ligands such as HMGB1, HSP and hyaluronan. Endogenous molecules bind to TLRs on DCs, macrophages and neutrophils that are recruited or infiltrated to injury sites and induce production of cytokines and chemokines and an inflammatory response.
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fig02: A proposed mechanism of inflammatory response in ischemia/reperfusion injury. Ischemia/reperfusion injury results in release of endogenous TLR ligands such as HMGB1, HSP and hyaluronan. Endogenous molecules bind to TLRs on DCs, macrophages and neutrophils that are recruited or infiltrated to injury sites and induce production of cytokines and chemokines and an inflammatory response.

Mentions: Ischemia/reperfusion injury is implicated in a broad array of pathological conditions such as myocardial infarction; cerebral stroke; and hepatic, renal and intestinal ischemia as well as following cardiovascular and transplant surgery [77]. The hallmark of these pathologies is extreme inflammation. Massive tissue injury with a large number of cells undergoing necrosis lead to the release of DAMPs from dead and dying cells resulting in the activation of TLRs and sterile inflammation (Fig. 2) [79]. Most of the evidence for the existence of endogenous TLR ligands is based on the study of I/R injury, the majority of endogenous ligands are likely to be involved in the activation of TLRs in I/R injury [80–82], but a strong necrosis-induced inflammatory response may, at least in part, be mediated by HMGB1 [83].


Endogenous toll-like receptor ligands and their biological significance.

Yu L, Wang L, Chen S - J. Cell. Mol. Med. (2010)

A proposed mechanism of inflammatory response in ischemia/reperfusion injury. Ischemia/reperfusion injury results in release of endogenous TLR ligands such as HMGB1, HSP and hyaluronan. Endogenous molecules bind to TLRs on DCs, macrophages and neutrophils that are recruited or infiltrated to injury sites and induce production of cytokines and chemokines and an inflammatory response.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4373479&req=5

fig02: A proposed mechanism of inflammatory response in ischemia/reperfusion injury. Ischemia/reperfusion injury results in release of endogenous TLR ligands such as HMGB1, HSP and hyaluronan. Endogenous molecules bind to TLRs on DCs, macrophages and neutrophils that are recruited or infiltrated to injury sites and induce production of cytokines and chemokines and an inflammatory response.
Mentions: Ischemia/reperfusion injury is implicated in a broad array of pathological conditions such as myocardial infarction; cerebral stroke; and hepatic, renal and intestinal ischemia as well as following cardiovascular and transplant surgery [77]. The hallmark of these pathologies is extreme inflammation. Massive tissue injury with a large number of cells undergoing necrosis lead to the release of DAMPs from dead and dying cells resulting in the activation of TLRs and sterile inflammation (Fig. 2) [79]. Most of the evidence for the existence of endogenous TLR ligands is based on the study of I/R injury, the majority of endogenous ligands are likely to be involved in the activation of TLRs in I/R injury [80–82], but a strong necrosis-induced inflammatory response may, at least in part, be mediated by HMGB1 [83].

Bottom Line: Toll-like receptors (TLRs), a family of pattern recognition receptors, recognize and respond to conserved components of microbes and play a crucial role in both innate and adaptive immunity.Putative endogenous TLR ligands include proteins and peptides, polysaccharides and proteoglycan, nucleic acids and phospholipids, which are cellular components, particularly extracellular matrix degradation products.The ability of TLRs to recognize endogenous stimulators appears to be essential to their function in regulating non-infectious inflammation.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, the First Affiliated Hospital, Sun Yat-sen (Zhongshan) University, Guangzhou, P.R. China.

Show MeSH
Related in: MedlinePlus