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  4. Microcrystals As Damps And Their Role In Joint Inflammation
 
  • Détails
Titre

Microcrystals As Damps And Their Role In Joint Inflammation

Type
abstract de conférence/colloque
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Série
Rheumatology
Auteur(s)
So, A.
Auteure/Auteur
Liens vers les personnes
So, Alexander Kai-Lik  
Liens vers les unités
Rhumatologie  
Titre du livre ou conférence/colloque
Annual Meeting of the British Society for Rheumatology
Adresse
Brighton, England, April 12-14, 2011
ISBN
1462-0324
Statut éditorial
Publié
Date de publication
2011
Volume
50
Première page
6
Dernière page/numéro d’article
7
Peer-reviewed
Oui
Langue
anglais
Notes
Publication type : Meeting Abstract
Résumé
The concept of danger signals as important triggers of inflammation and immune activation has passed from fanciful hypothesis to a widely accepted biological process with receptors, signalling cascades and mediators. Products of cell death or cell stress are prime examples of DAMPs. They interact with receptors on the cell surface such as TLRs as well as cytoplasmic proteins such as the NLRs to modulate cellular metabolism and activation. Recently, the identification of the inflammasomes and their role in processing IL-1b and IL18 provided further insights into how DAMPs provoke inflammation. A class of substances that are potent activators of the inflammasome is microcrystals. All three microcrystals associated with joint disease in man : urate, CPP and hydroxyapatite require the NLRP3 inflammasome to process and release IL-1b from leucocytes. This mechanism most probably explain the inflammatory phase of acute crystal arthritis. However, microcrystals can also induce apoptosis, cell death as well as cell activation, depending on the cell type they are in contact with. These different cellular effects could well explain the role crystals can play in degenerative joint diseases, where inflammation is not as prominent. Our understanding of the intracellular pathways linking microcrystals to inflammation and cell activation is currently still very sketchy, and we hope that the detailed analysis of these pathways may lead to better comprehension and treatment of microcrystal induced joint diseases.Disclosures : The author has declared no conflicts of interest.
PID Serval
serval:BIB_714118882F12
WOS
000289163800026
Permalien
https://iris.unil.ch/handle/iris/219814
Date de création
2011-05-06T14:16:40.482Z
Date de création dans IRIS
2025-05-21T04:12:30Z
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