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Toll-Like Receptor Stimulation Induces Higher TNF-α Secretion in Peripheral Blood Mononuclear Cells from Patients with Hyper IgE Syndrome

by Litzman, Jiri , Ehl, Stephan , Yeganeh, Mehdi , Thiel, Doerte , Kilic, Sara S. , Espanol, Teresa , Renner, Ellen , Rothenfusser, Simon , Rezaei, Nima , Plebani, Alessandro , Grimbacher, Bodo , Hawn, Thomas R. , Pietrogrande, Cristina , Matamoros, Nuria , Sanal, Ozden , Breborowicz, Anna , Franco, Jose L. , Henneke, Philipp , Woellner, Cristina

in 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

2008

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Toll-Like Receptor Stimulation Induces Higher TNF-α Secretion in Peripheral Blood Mononuclear Cells from Patients with Hyper IgE Syndrome

2008

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Toll-Like Receptor Stimulation Induces Higher TNF-α Secretion in Peripheral Blood Mononuclear Cells from Patients with Hyper IgE Syndrome

2008

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Journal Article

Toll-Like Receptor Stimulation Induces Higher TNF-α Secretion in Peripheral Blood Mononuclear Cells from Patients with Hyper IgE Syndrome

Litzman, Jiri,

Ehl, Stephan,

Yeganeh, Mehdi,

Thiel, Doerte,

Kilic, Sara S.,

Espanol, Teresa,

Renner, Ellen,

Rothenfusser, Simon,

Rezaei, Nima,

Plebani, Alessandro,

Grimbacher, Bodo,

Hawn, Thomas R.,

Pietrogrande, Cristina,

Matamoros, Nuria,

Sanal, Ozden,

Breborowicz, Anna,

Franco, Jose L.,

Henneke, Philipp,

Woellner, Cristina

2008

Overview

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.

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Publisher

Karger

Subject

Biological and medical sciences

/ Cohort Studies

/ Female

/ Fundamental and applied biological sciences. Psychology

/ Fundamental immunology

/ Humans

/ Immunodeficiencies