Toll-like receptor activation in the pathogenesis of lupus nephritis

Copyright © 2016 Elsevier Inc. All rights reserved.

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 185(2017) vom: 16. Dez., Seite 86-94
Auteur principal: Lorenz, Georg (Auteur)
Autres auteurs: Lech, Maciej, Anders, Hans-Joachim
Format: Article en ligne
Langue:English
Publié: 2017
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Review Research Support, Non-U.S. Gov't Antiviral Glomerulonephritis Immune complex Innate immunity Therapy Toll-Like Receptors
Description
Résumé:Copyright © 2016 Elsevier Inc. All rights reserved.
The pathogenesis of systemic lupus erythematosus (SLE) and lupus nephritis is complex but no longer enigmatic. Much progress has been made to on the polygenetic origin of lupus in identifying gene variants that permit the loss of tolerance against nuclear autoantigens. Along the same line in about 50% of lupus patients additional genetic weaknesses promote immune complex glomerulonephritis and filtration barrier dysfunction. Here we briefly summarize the pathogenesis of SLE with a focus on loss of tolerance and the role of toll-like receptors in the "pseudo"-antiviral immunity concept of systemic lupus. In addition, we discuss the local role of Toll-like receptors in intrarenal inflammation and kidney remodeling
Description:Date Completed 29.11.2017
Date Revised 06.02.2018
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2016.07.015