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

Clin Immunol. 2013 Mar;146(3):165-75. doi: 10.1016/j.clim.2012.12.009. Epub 2013 Jan 3.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylation
  • Adolescent
  • Adult
  • Cytokines / blood
  • Cytokines / genetics
  • Female
  • GATA3 Transcription Factor
  • Hepatitis A Virus Cellular Receptor 1
  • Histones / metabolism*
  • Humans
  • IgA Vasculitis / immunology
  • IgA Vasculitis / metabolism*
  • Leukocytes, Mononuclear / cytology
  • Leukocytes, Mononuclear / metabolism*
  • Male
  • Membrane Glycoproteins
  • Methylation
  • Middle Aged
  • RNA, Messenger / metabolism
  • Receptors, Virus
  • T-Lymphocyte Subsets / immunology
  • Young Adult

Substances

  • Cytokines
  • GATA3 Transcription Factor
  • GATA3 protein, human
  • HAVCR1 protein, human
  • Hepatitis A Virus Cellular Receptor 1
  • Histones
  • Membrane Glycoproteins
  • RNA, Messenger
  • Receptors, Virus