Toll-like receptor stimulation induces higher TNF-alpha secretion in peripheral blood mononuclear cells from patients with hyper IgE syndrome.

Yeganeh M., Henneke P., Rezaei N., Ehl S., Thiel D., Matamoros N., ...More

International archives of allergy and immunology, vol.146, no.3, pp.190-4, 2008 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 146 Issue: 3
  • Publication Date: 2008
  • Doi Number: 10.1159/000115886
  • Journal Name: International archives of allergy and immunology
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.190-4
  • Keywords: hyper IgE syndrome, toll-like receptor, TNF-alpha, TUMOR-NECROSIS-FACTOR, DEFICIENCY, SIGNALS, INNATE
  • Bursa Uludag University Affiliated: Yes


Hyper IgE syndromes (HIES) are primary immunodeficiency disorders of unknown pathogenesis. Patients are typically affected with 'cold' abscesses of the skin, recurrent cyst-forming pneumonia, chronic mucocutaneous candidiasis and other less frequent features such as progressive skeletal abnormalities. Defective signaling in the Toll-like receptor (TLR) pathways has been suggested as a responsible pathologic mechanism, however, in previous reports, 10 patients revealed no defect in inflammatory cytokine responses to different TLR ligands. Here, we report the increase in pro-inflammatory cytokines TNF-alpha and IL-8, following TLR2 and TLR4 stimulation in a larger cohort of 25 additional patients with HIES, and provide a meta-analysis of the TLR data in HIES. Copyright (C) 2008 S. Karger AG, Basel.