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

Abstract

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.

• Authors: Mehdi Yeganeh, Philipp Henneke, Nima Rezaei, Stephan Ehl, Doerte Thiel, Nuria Matamoros, Cristina Pietrogrande, Teresa Espanol, Jiri Litzman, Jose L Franco, Ozden Sanal, Sara S Kilic, Anna Breborowicz, Alessandro Plebani, Ellen Renner, Simon Rothenfusser, Thomas R Hawn, Cristina Woellner, Bodo Grimbacher
• Journal: International archives of allergy and immunology (Int Arch Allergy Immunol) Vol. 146 Issue 3 Pg. 190-4 ( 2008) ISSN: 1423-0097 [Electronic] Switzerland
• PMID: 18268386 (Publication Type: Journal Article, Multicenter Study, Research Support, Non-U.S. Gov't)
• Copyright: (c) 2008 S. Karger AG, Basel

Chemical References

• Interleukin-8
• Lipopolysaccharides
• TLR2 protein, human
• TLR4 protein, human
• Toll-Like Receptor 2
• Toll-Like Receptor 4
• Tumor Necrosis Factor-alpha

Topics

• Cohort Studies
• Female
• Humans
• Interleukin-8 (blood, immunology)
• Job Syndrome (immunology)
• Leukocytes, Mononuclear (immunology)
• Lipopolysaccharides (immunology)
• Male
• Signal Transduction
• Statistics, Nonparametric
• Toll-Like Receptor 2 (immunology)
• Toll-Like Receptor 4 (immunology)
• Tumor Necrosis Factor-alpha (blood, immunology)