Aberrant histone modifications in peripheral blood mononuclear cells from patients with Henoch-Schönlein purpura

Copyright © 2013 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 146(2013), 3 vom: 05. März, Seite 165-75
1. Verfasser: Luo, Shuangyan (VerfasserIn)
Weitere Verfasser: Liang, Gongping, Zhang, Peng, Zhao, Ming, Lu, Qianjin
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2013
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Cytokines GATA3 Transcription Factor GATA3 protein, human HAVCR1 protein, human Hepatitis A Virus Cellular Receptor 1 Histones Membrane Glycoproteins RNA, Messenger Receptors, Virus
Beschreibung
Zusammenfassung:Copyright © 2013 Elsevier Inc. All rights reserved.
Henoch-Schönlein purpura (HSP), the most common type of leukocytoclastic vasculitis, is caused by T cell-mediated autoimmune reactions. In this study, we analyze histone modification patterns in peripheral blood mononuclear cells (PBMCs) of HSP patients, and investigate the expression levels of inflammatory cytokines (IFN-γ, IL-2, IL-4, IL-6 and IL-13), transcription factors (T-bet, GATA-3 and TIM-1) and chemokines (CXCL4 and CXCL10) in HSP patients. Our results show that histone H3 acetylation and methylation are significantly enhanced in PBMCs from HSP patients. We also demonstrate specifically that marked increases in histone H3 acetylation and H3 lysine 4 trimethylation occur at the IL-4 loci in these patients. In addition, the expression levels of IL-4, IL-6, IL-13, GATA-3, TIM-1 and CXCL4 are also increased. These findings suggest that abnormal histone modifications are present in the PBMCs of patients with HSP, possibly contributing to the activation of pathological immune responses associated with HSP
Beschreibung:Date Completed 23.04.2013
Date Revised 09.04.2022
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2012.12.009