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

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

doi:10.1159/000115886

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

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

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	190-194
Number of pages	5
Journal	International Archives of Allergy and Immunology
Volume	146
Issue number	3
DOIs	https://doi.org/10.1159/000115886
State	Published - Jun 2008
Externally published	Yes

Keywords

Hyper IgE syndrome
TNF-α
Toll-like receptor

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10.1159/000115886

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Yeganeh, M., Henneke, P., Rezaei, N., Ehl, S., Thiel, D., Matamoros, N., Pietrogrande, C., Espanol, T., Litzman, J., Franco, J. L., Sanal, O., Kilic, S. S., Breborowicz, A., Plebani, A., Renner, E., Rothenfusser, S., Hawn, T. R., Woellner, C., & Grimbacher, B. (2008). Toll-like receptor stimulation induces higher TNF-α secretion in peripheral blood mononuclear cells from patients with hyper IgE syndrome. International Archives of Allergy and Immunology, 146(3), 190-194. https://doi.org/10.1159/000115886

@article{ef32cd558d06424a8b6eef2ead26cc64,

title = "Toll-like receptor stimulation induces higher TNF-α secretion in peripheral blood mononuclear cells from patients with hyper IgE syndrome",

abstract = "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.",

keywords = "Hyper IgE syndrome, TNF-α, Toll-like receptor",

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

year = "2008",

month = jun,

doi = "10.1159/000115886",

language = "English",

volume = "146",

pages = "190--194",

journal = "International Archives of Allergy and Immunology",

issn = "1018-2438",

publisher = "S. Karger AG",

number = "3",

}

Yeganeh, M, Henneke, P, Rezaei, N, Ehl, S, Thiel, D, Matamoros, N, Pietrogrande, C, Espanol, T, Litzman, J, Franco, JL, Sanal, O, Kilic, SS, Breborowicz, A, Plebani, A, Renner, E, Rothenfusser, S, Hawn, TR, Woellner, C & Grimbacher, B 2008, 'Toll-like receptor stimulation induces higher TNF-α secretion in peripheral blood mononuclear cells from patients with hyper IgE syndrome', International Archives of Allergy and Immunology, vol. 146, no. 3, pp. 190-194. https://doi.org/10.1159/000115886

TY - JOUR

T1 - Toll-like receptor stimulation induces higher TNF-α secretion in peripheral blood mononuclear cells from patients with hyper IgE syndrome

AU - Yeganeh, Mehdi

AU - Henneke, Philipp

AU - Rezaei, Nima

AU - Ehl, Stephan

AU - Thiel, Doerte

AU - Matamoros, Nuria

AU - Pietrogrande, Cristina

AU - Espanol, Teresa

AU - Litzman, Jiri

AU - Franco, Jose L.

AU - Sanal, Ozden

AU - Kilic, Sara S.

AU - Breborowicz, Anna

AU - Plebani, Alessandro

AU - Renner, Ellen

AU - Rothenfusser, Simon

AU - Hawn, Thomas R.

AU - Woellner, Cristina

AU - Grimbacher, Bodo

PY - 2008/6

Y1 - 2008/6

N2 - 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.

AB - 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.

KW - Hyper IgE syndrome

KW - TNF-α

KW - Toll-like receptor

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U2 - 10.1159/000115886

DO - 10.1159/000115886

M3 - Article

C2 - 18268386

AN - SCOPUS:45149083315

SN - 1018-2438

VL - 146

SP - 190

EP - 194

JO - International Archives of Allergy and Immunology

JF - International Archives of Allergy and Immunology

IS - 3

ER -

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

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Keywords

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