Yeganeh, MehdiHenneke, PhilippRezaei, NimaEhl, StephanThiel, DoerteMatamoros, NuriaPietrogrande, CristinaEspanol, TeresaLitzman, JiriFranco, Jose L.Sanal, OzdenKılıç, Sara S.Breborowicz, AnnaPlebani, AlessandroRenner, EllenRothenfusser, SimonHawn, Thomas R.Woellner, CristinaGrimbacher, Bodo2024-11-062024-11-062008-01-011018-2438https://doi.org/10.1159/000115886https://karger.com/iaa/article/146/3/190/165542/Toll-Like-Receptor-Stimulation-Induces-Higher-TNFhttps://hdl.handle.net/11452/47475Hyper 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.eninfo:eu-repo/semantics/openAccessTumor-necrosis-factorDeficiencySignalsInnateHyper ige syndromeToll-like receptorTnf-alphaAllergyImmunologyArticle000255896000002190194146310.1159/000115886