FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2065616962> ?p ?o ?g. }

• W2065616962 endingPage "e1004050" @default.
• W2065616962 startingPage "e1004050" @default.
• W2065616962 abstract "Chitin is an essential structural polysaccharide of fungal pathogens and parasites, but its role in human immune responses remains largely unknown. It is the second most abundant polysaccharide in nature after cellulose and its derivatives today are widely used for medical and industrial purposes. We analysed the immunological properties of purified chitin particles derived from the opportunistic human fungal pathogen Candida albicans, which led to the selective secretion of the anti-inflammatory cytokine IL-10. We identified NOD2, TLR9 and the mannose receptor as essential fungal chitin-recognition receptors for the induction of this response. Chitin reduced LPS-induced inflammation in vivo and may therefore contribute to the resolution of the immune response once the pathogen has been defeated. Fungal chitin also induced eosinophilia in vivo, underpinning its ability to induce asthma. Polymorphisms in the identified chitin receptors, NOD2 and TLR9, predispose individuals to inflammatory conditions and dysregulated expression of chitinases and chitinase-like binding proteins, whose activity is essential to generate IL-10-inducing fungal chitin particles in vitro, have also been linked to inflammatory conditions and asthma. Chitin recognition is therefore critical for immune homeostasis and is likely to have a significant role in infectious and allergic disease. Authors Summary Chitin is the second most abundant polysaccharide in nature after cellulose and an essential component of the cell wall of all fungal pathogens. The discovery of human chitinases and chitinase-like binding proteins indicates that fungal chitin is recognised by cells of the human immune system, shaping the immune response towards the invading pathogen. We show that three immune cell receptors– the mannose receptor, NOD2 and TLR9 recognise chitin and act together to mediate an anti-inflammatory response via secretion of the cytokine IL-10. This mechanism may prevent inflammation-based damage during fungal infection and restore immune balance after an infection has been cleared. By increasing the chitin content in the cell wall pathogenic fungi may influence the immune system in their favour, by down-regulating protective inflammatory immune responses. Furthermore, gene mutations and dysregulated enzyme activity in the described chitin recognition pathway are implicated in inflammatory conditions such as Crohn's Disease and asthma, highlighting the importance of the discovered mechanism in human health." @default.
• W2065616962 created "2016-06-24" @default.
• W2065616962 creator A5004410792 @default.
• W2065616962 creator A5008227126 @default.
• W2065616962 creator A5012575652 @default.
• W2065616962 creator A5019826825 @default.
• W2065616962 creator A5027955775 @default.
• W2065616962 creator A5039813701 @default.
• W2065616962 creator A5049039015 @default.
• W2065616962 creator A5069868013 @default.
• W2065616962 creator A5074251335 @default.
• W2065616962 creator A5078265837 @default.
• W2065616962 creator A5079550119 @default.
• W2065616962 creator A5083942054 @default.
• W2065616962 creator A5088189848 @default.
• W2065616962 date "2014-04-10" @default.
• W2065616962 modified "2023-10-16" @default.
• W2065616962 title "Fungal Chitin Dampens Inflammation through IL-10 Induction Mediated by NOD2 and TLR9 Activation" @default.
• W2065616962 cites W1672848901 @default.
• W2065616962 cites W1945479327 @default.
• W2065616962 cites W1964687996 @default.
• W2065616962 cites W1964923650 @default.
• W2065616962 cites W1971909186 @default.
• W2065616962 cites W1980210558 @default.
• W2065616962 cites W1990215850 @default.
• W2065616962 cites W1995479601 @default.
• W2065616962 cites W1999206690 @default.
• W2065616962 cites W2000418701 @default.
• W2065616962 cites W2002367129 @default.
• W2065616962 cites W2002612766 @default.
• W2065616962 cites W2010247691 @default.
• W2065616962 cites W2014225024 @default.
• W2065616962 cites W2025131995 @default.
• W2065616962 cites W2031222013 @default.
• W2065616962 cites W2038204439 @default.
• W2065616962 cites W2039557932 @default.
• W2065616962 cites W2040773127 @default.
• W2065616962 cites W2044322945 @default.
• W2065616962 cites W2051893297 @default.
• W2065616962 cites W2052690587 @default.
• W2065616962 cites W2064255099 @default.
• W2065616962 cites W2065581418 @default.
• W2065616962 cites W2065628251 @default.
• W2065616962 cites W2075045438 @default.
• W2065616962 cites W2083119828 @default.
• W2065616962 cites W2083351672 @default.
• W2065616962 cites W2086193922 @default.
• W2065616962 cites W2093217993 @default.
• W2065616962 cites W2093424190 @default.
• W2065616962 cites W2096857575 @default.
• W2065616962 cites W2100604737 @default.
• W2065616962 cites W2103174126 @default.
• W2065616962 cites W2107794472 @default.
• W2065616962 cites W2111910963 @default.
• W2065616962 cites W2113573651 @default.
• W2065616962 cites W2115618383 @default.
• W2065616962 cites W2124424645 @default.
• W2065616962 cites W2126540424 @default.
• W2065616962 cites W2130963153 @default.
• W2065616962 cites W2139584811 @default.
• W2065616962 cites W2144014442 @default.
• W2065616962 cites W2151045435 @default.
• W2065616962 cites W2153207137 @default.
• W2065616962 cites W2160451358 @default.
• W2065616962 cites W2165154646 @default.
• W2065616962 cites W2308911018 @default.
• W2065616962 cites W48578805 @default.
• W2065616962 doi "https://doi.org/10.1371/journal.ppat.1004050" @default.
• W2065616962 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3983064" @default.
• W2065616962 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24722226" @default.
• W2065616962 hasPublicationYear "2014" @default.
• W2065616962 type Work @default.
• W2065616962 sameAs 2065616962 @default.
• W2065616962 citedByCount "206" @default.
• W2065616962 countsByYear W20656169622014 @default.
• W2065616962 countsByYear W20656169622015 @default.
• W2065616962 countsByYear W20656169622016 @default.
• W2065616962 countsByYear W20656169622017 @default.
• W2065616962 countsByYear W20656169622018 @default.
• W2065616962 countsByYear W20656169622019 @default.
• W2065616962 countsByYear W20656169622020 @default.
• W2065616962 countsByYear W20656169622021 @default.
• W2065616962 countsByYear W20656169622022 @default.
• W2065616962 countsByYear W20656169622023 @default.
• W2065616962 crossrefType "journal-article" @default.
• W2065616962 hasAuthorship W2065616962A5004410792 @default.
• W2065616962 hasAuthorship W2065616962A5008227126 @default.
• W2065616962 hasAuthorship W2065616962A5012575652 @default.
• W2065616962 hasAuthorship W2065616962A5019826825 @default.
• W2065616962 hasAuthorship W2065616962A5027955775 @default.
• W2065616962 hasAuthorship W2065616962A5039813701 @default.
• W2065616962 hasAuthorship W2065616962A5049039015 @default.
• W2065616962 hasAuthorship W2065616962A5069868013 @default.
• W2065616962 hasAuthorship W2065616962A5074251335 @default.
• W2065616962 hasAuthorship W2065616962A5078265837 @default.
• W2065616962 hasAuthorship W2065616962A5079550119 @default.
• W2065616962 hasAuthorship W2065616962A5083942054 @default.
• W2065616962 hasAuthorship W2065616962A5088189848 @default.

• next