Toll-like receptor stimulation induces higher TNF-alpha secretion in peripheral blood mononuclear cells from patients with hyper IgE syndrome.
International archives of allergy and immunology, cilt.146, sa.3, ss.190-4, 2008 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 146 Sayı: 3
- Basım Tarihi: 2008
- Doi Numarası: 10.1159/000115886
- Dergi Adı: International archives of allergy and immunology
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.190-4
- Anahtar Kelimeler: hyper IgE syndrome, toll-like receptor, TNF-alpha, TUMOR-NECROSIS-FACTOR, DEFICIENCY, SIGNALS, INNATE
- Bursa Uludağ Üniversitesi Adresli: Evet
Özet
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.