Estrogen receptor alpha modulates Toll-like receptor signaling in murine lupus

Copyright © 2012. Published by Elsevier Inc.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 144(2012), 1 vom: 27. Juli, Seite 1-12
1. Verfasser: Cunningham, Melissa A (VerfasserIn)
Weitere Verfasser: Naga, Osama S, Eudaly, Jackie G, Scott, Jennifer L, Gilkeson, Gary S
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2012
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Cytokines Estrogen Receptor alpha Toll-Like Receptors Guanosine 12133JR80S loxoribine 9CAS0V66OI
Beschreibung
Zusammenfassung:Copyright © 2012. Published by Elsevier Inc.
Systemic lupus erythematosus (SLE) is a disease that disproportionately affects females. Despite significant research effort, the mechanisms underlying the female predominance in this disease are largely unknown. Previously, we showed that estrogen receptor alpha knockout (ERαKO) lupus prone female mice had significantly less pathologic renal disease and proteinuria, and significantly prolonged survival. Since autoantibody levels and number and percentage of B/T cells were not significantly impacted by ERα genotype, we hypothesized that the primary benefit of ERα deficiency in lupus nephritis was via modulation of the innate immune response. Using BMDCs and spleen cells/B cells from female wild-type or ERαKO mice, we found that ERαKO-derived cells have a significantly reduced inflammatory response after stimulation with TLR agonists. Our results indicate that the inflammatory response to TLR ligands is significantly impacted by the presence of ERα despite the absence of estradiol, and may partially explain the protective effect of ERα deficiency in lupus-prone animals
Beschreibung:Date Completed 23.08.2012
Date Revised 21.10.2021
published: Print-Electronic
CommentIn: Clin Immunol. 2012 Jul;144(1):53-6. - PMID 22659035
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2012.04.001