Detailed Information on Publication Record
2008
Toll-like receptor stimulation induces higher TNF-alpha secretion in peripheral blood mononuclear cells from patients with hyper IgE syndrome.
YEGANEH, Mehdi, Philip HENNEKE, Nima REZAEI, Stephan EHL, Doerte THIEL et. al.Basic information
Original name
Toll-like receptor stimulation induces higher TNF-alpha secretion in peripheral blood mononuclear cells from patients with hyper IgE syndrome.
Name in Czech
Stimulace Toll-like receptorů periferních mononukleárů pacientů s hyper IgE syndromem vede k tvorbě TNF alfa
Authors
YEGANEH, Mehdi (364 Islamic Republic of Iran), Philip HENNEKE (276 Germany), Nima REZAEI (364 Islamic Republic of Iran), Stephan EHL (276 Germany), Doerte THIEL (276 Germany), Nuria MATAMOROS (724 Spain), Cristina PIETROGRADA (380 Italy), Teresa ESPANOL (724 Spain), Jiří LITZMAN (203 Czech Republic, guarantor), Jose L. FRANCO (170 Colombia), Ozden SANAL (792 Turkey), Sara S. KILIC (792 Turkey), Anna BREBOROWICZ (792 Turkey), Alessandro BLEBANI (380 Italy), Ellen RENNER (276 Germany), Simon ROTHENFUSSER (276 Germany), Thomas R. RAWN (840 United States of America), Cristina WOELLNER (826 United Kingdom of Great Britain and Northern Ireland) and Bodo GRIMBACHER (826 United Kingdom of Great Britain and Northern Ireland)
Edition
International Archives Allergy and Immunology, Basel, Karger AG, 2008, 1018-2438
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30102 Immunology
Country of publisher
Switzerland
Confidentiality degree
není předmětem státního či obchodního tajemství
Impact factor
Impact factor: 2.131
RIV identification code
RIV/00216224:14110/08:00028225
Organization unit
Faculty of Medicine
UT WoS
000255896000002
Keywords in English
Hyper IgE syndrome; Toll-like receptor;TNF alpha
Tags
International impact, Reviewed
Změněno: 2/4/2010 08:03, prof. MUDr. Jiří Litzman, CSc.
V originále
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.
In Czech
Stimulace Toll-like receptorů periferních mononukleárů pacientů s hyper IgE syndromem vede k tvorbě TNF alfa
Links
NR9192, research and development project |
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