Titre
Mechanisms of airway obliteration after lung transplantation.
Type
synthèse (review)
Institution
Externe
Périodique
Proceedings of the American Thoracic Society
Auteur(s)
Nicod, L.P.
Auteure/Auteur
Liens vers les personnes
ISSN
1546-3222[print], 1546-3222[linking]
Statut éditorial
Publié
Date de publication
2006
Volume
3
Numéro
5
Première page
444
Dernière page/numéro d’article
449
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Résumé
Post-transplant bronchiolitis obliterans, also called bronchiolitis obliterans syndrome, affects up to 50-60% of patients who survive 5 yr after surgery according to its clinical definition, which is based on the degree of obstructive airway disease. Alloimmune-independent and -dependent mechanisms produce injuries and inflammation of epithelial cells and subepithelial structures, leading to aberrant tissue repair. The triggering of innate immunity by various infections or chemical injuries after, for example, gastroesophageal reflux, may lead to the release of danger signals that are able to activate dendritic cells, a crucial link with adaptive immunity. Inflammation can also increase the expression and display of major histocompatibility alloantigens and thus favor the initiation of rejection episodes. These phenomena may be limited in time and location or may be protracted. Reducing the risk of alloimmune-independent factors may be as important as treating acute episodes of lung rejection. Excessive immunosuppression may be deleterious by increasing the risk of infection, thereby triggering innate and adaptive immunity. New potential therapeutic targets are emerging from the research performed on leukotriene receptors, chemokine receptors, and growth factors. Neutralizing these molecules reduces the initial mononuclear and polynuclear infiltrates or the subsequent fibroproliferative process and the neovascular changes, feeding this process.
PID Serval
serval:BIB_132E0F9C496F
PMID
Date de création
2010-02-19T18:18:26.210Z
Date de création dans IRIS
2025-05-20T20:02:48Z