Indoleamine-2,3-dioxygenase in murine and human systemic lupus erythematosus : Down-regulation by the tolerogeneic peptide hCDR1

Copyright © 2018 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 197(2018) vom: 01. Dez., Seite 34-39
1. Verfasser: Sthoeger, Zev (VerfasserIn)
Weitere Verfasser: Sharabi, Amir, Zinger, Heidy, Asher, Ilan, Mozes, Edna
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2018
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Cytokines FOXP3 Immunomodulation of gene expression Indoleamine 2,3-dioxygenase (IDO) Systemic lupus erythematosus (SLE) Tolerogenic peptide (hCDR1) Antibodies, Monoclonal FOXP3 protein, human Forkhead Transcription Factors mehr... Foxp3 protein, mouse Indoleamine-Pyrrole 2,3,-Dioxygenase Peptide Fragments edratide 38PLP07BKC
Beschreibung
Zusammenfassung:Copyright © 2018 Elsevier Inc. All rights reserved.
וֹndoleamine-2,3-dioxygenase (IDO) plays a role in immune regulation. Increased IDO activity was reported in systemic lupus erythematosus (SLE). We investigated the effects of the tolerogenic peptide hCDR1, shown to ameliorate lupus manifestations, on IDO gene expression. mRNA was prepared from splenocytes of hCDR1- treated SLE-afflicted (NZBxNZW)F1 mice, from blood samples of lupus patients, collected before and after their in vivo treatment with hCDR1 and from peripheral blood mononuclear cells (PBMC) of patients incubated with hCDR1. IDO gene expression was determined by real-time RT-PCR. hCDR1 significantly down-regulated IDO expression in SLE-affected mice and in lupus patients (treated in vivo and in vitro). No effects were observed in healthy donors or following treatment with a control peptide. Diminished IDO gene expression was associated with hCDR1 beneficial effects. Our results suggest that the hCDR1-induced FOXP3 expressing regulatory T cells in lupus are not driven by IDO but rather by other hCDR1 regulated pathways
Beschreibung:Date Completed 07.10.2019
Date Revised 07.10.2019
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2018.08.012