Toll-Like Receptor Stimulation Induces Higher TNF-α Secretion in Peripheral Blood Mononuclear Cells from Patients with Hyper IgE Syndrome
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 abnormalitie...
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| Veröffentlicht in: | International archives of allergy and immunology 2008-01, Vol.146 (3), p.190-194 |
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| creator | Yeganeh, Mehdi Henneke, Philipp Rezaei, Nima Ehl, Stephan Thiel, Doerte Matamoros, Nuria Pietrogrande, Cristina Espanol, Teresa Litzman, Jiri Franco, Jose L. Sanal, Ozden Kilic, Sara S. Breborowicz, Anna Plebani, Alessandro Renner, Ellen Rothenfusser, Simon Hawn, Thomas R. Woellner, Cristina Grimbacher, Bodo |
| description | 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-α 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. |
| doi_str_mv | 10.1159/000115886 |
| format | Article |
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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-α 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.</description><identifier>ISSN: 1018-2438</identifier><identifier>EISSN: 1423-0097</identifier><identifier>DOI: 10.1159/000115886</identifier><identifier>PMID: 18268386</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Biological and medical sciences ; Cohort Studies ; Female ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Humans ; Immunodeficiencies ; Immunodeficiencies. Immunoglobulinopathies ; Immunopathology ; Interleukin-8 - blood ; Interleukin-8 - immunology ; Job Syndrome - immunology ; Leukocytes, Mononuclear - immunology ; Lipopolysaccharides - immunology ; Male ; Medical sciences ; Original Paper ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Signal Transduction ; Statistics, Nonparametric ; Toll-Like Receptor 2 - immunology ; Toll-Like Receptor 4 - immunology ; Tumor Necrosis Factor-alpha - blood ; Tumor Necrosis Factor-alpha - immunology</subject><ispartof>International archives of allergy and immunology, 2008-01, Vol.146 (3), p.190-194</ispartof><rights>2008 S. Karger AG, Basel</rights><rights>2008 INIST-CNRS</rights><rights>(c) 2008 S. 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| subjects | Biological and medical sciences Cohort Studies Female Fundamental and applied biological sciences. Psychology Fundamental immunology Humans Immunodeficiencies Immunodeficiencies. Immunoglobulinopathies Immunopathology Interleukin-8 - blood Interleukin-8 - immunology Job Syndrome - immunology Leukocytes, Mononuclear - immunology Lipopolysaccharides - immunology Male Medical sciences Original Paper Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Signal Transduction Statistics, Nonparametric Toll-Like Receptor 2 - immunology Toll-Like Receptor 4 - immunology Tumor Necrosis Factor-alpha - blood Tumor Necrosis Factor-alpha - immunology |
| title | Toll-Like Receptor Stimulation Induces Higher TNF-α Secretion in Peripheral Blood Mononuclear Cells from Patients with Hyper IgE Syndrome |
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