Phenotype and function of dendritic cells of patients with systemic lupus erythematosus

Copyright © 2011 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 143(2012), 1 vom: 12. Apr., Seite 45-50
1. Verfasser: Crispín, José C (VerfasserIn)
Weitere Verfasser: Vargas-Rojas, Maria Ines, Monsiváis-Urenda, Adriana, Alcocer-Varela, Jorge
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2012
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't B7-1 Antigen B7-2 Antigen CD80-CAP Interleukin-6 Lipopolysaccharides Oligopeptides Tumor Necrosis Factor-alpha Interleukin-10 mehr... 130068-27-8 Dinoprostone K7Q1JQR04M
Beschreibung
Zusammenfassung:Copyright © 2011 Elsevier Inc. All rights reserved.
Dendritic cells (DC) regulate the activation and differentiation of T cells. They are activated by signals of inflammation and tissue damage, and thus could play a role in the amplification and perpetuation of autoimmune diseases such as systemic lupus erythematosus (SLE). Here we analyzed the phenotype of circulating DC from patients with SLE and studied their differentiation from monocytes. Peripheral blood DC exhibited increased levels of activation in patients with SLE. Although their in vitro differentiation process occurred normally, their responses to activation stimuli (LPS, TNF-α plus PGE(2), anti-CD40) were abnormal when compared to DC differentiated from healthy monocytes. When incubated in the presence of IL-10, DC from patients with SLE were able to induce tolerance to allogeneic antigens in a normal manner. Our results suggest that DC from patients with SLE are abnormal, in part due to the effect of abundant pro-inflammatory signals, but also because of intrinsic cellular defects that alter their responses to activation stimuli
Beschreibung:Date Completed 11.05.2012
Date Revised 16.11.2017
published: Print-Electronic
CommentIn: Clin Immunol. 2012 Apr;143(1):4-5. doi: 10.1016/j.clim.2012.01.006. - PMID 22326124
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2011.12.004