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

M Yeganeh, P Henneke, N Rezaei, S Ehl, D Thiel, N Matamoros, C Pietrogrande, T Espanol, J Litzman, JL Franco, O Sanal, SS Kilic, A Breborowicz, A Plebani, E Renner, S Rothenfusser, TR Hawn, C Woellner, B Grimbacher

. 2008 ; 146 (3) : 190-194.

Language English Country Switzerland

Document type Multicenter Study, Research Support, Non-U.S. Gov't

Grant support
NR9192 MZ0 CEP Register

Digital library NLK
Full text - Část
Source

E-resources Online Full text

NLK Karger Journals from 1992 to 2009
ProQuest Central from 1998-01-01 to 2015-12-31
Medline Complete (EBSCOhost) from 1998-01-01 to 1 year ago
Health & Medicine (ProQuest) from 1998-01-01 to 2015-12-31

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. (c) 2008 S. Karger AG, Basel

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