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Statements

Subject Item
n2:RIV%2F00216208%3A11130%2F11%3A7091%21RIV12-MZ0-11130___
rdf:type
skos:Concept n11:Vysledek
rdfs:seeAlso
http://www.ncbi.nlm.nih.gov/pubmed/21910722
dcterms:description
Hyper-immunoglobulin (Ig) E syndrome (HIES) is a primary immunodeficiency associated with mutations in STAT3 resulting in impaired development of T helper type 17 (Th17) lymphocytes. HIES patients with a reduced frequency of Th17 cells present with infections caused by Staphylococcus aureus and/or Candida strains. The same spectrum of pathogens is present in patients with chronic granulomatous disease (CGD). We analysed the characteristics of the Th17 compartment in HIES and CGD. HIES patients showed very low numbers of Th17 cells. By contrast, the frequency of Th17 cells and production of Th17-derived cytokines was significantly higher among CGD patients when compared to both control samples and HIES. Naive CD4(+) cells in CGD patients had a normal capacity to differentiate into IL-17-producing cells and the numbers of Th17 cells in the CGD patients normalized following successful bone marrow transplantation. Our findings complement recent data on the importance of Th17 cells for elimination of infections with C. albicans and S. aureus. Hyper-immunoglobulin (Ig) E syndrome (HIES) is a primary immunodeficiency associated with mutations in STAT3 resulting in impaired development of T helper type 17 (Th17) lymphocytes. HIES patients with a reduced frequency of Th17 cells present with infections caused by Staphylococcus aureus and/or Candida strains. The same spectrum of pathogens is present in patients with chronic granulomatous disease (CGD). We analysed the characteristics of the Th17 compartment in HIES and CGD. HIES patients showed very low numbers of Th17 cells. By contrast, the frequency of Th17 cells and production of Th17-derived cytokines was significantly higher among CGD patients when compared to both control samples and HIES. Naive CD4(+) cells in CGD patients had a normal capacity to differentiate into IL-17-producing cells and the numbers of Th17 cells in the CGD patients normalized following successful bone marrow transplantation. Our findings complement recent data on the importance of Th17 cells for elimination of infections with C. albicans and S. aureus.
dcterms:title
Expansion of T helper type 17 lymphocytes in patients with chronic granulomatous disease Expansion of T helper type 17 lymphocytes in patients with chronic granulomatous disease
skos:prefLabel
Expansion of T helper type 17 lymphocytes in patients with chronic granulomatous disease Expansion of T helper type 17 lymphocytes in patients with chronic granulomatous disease
skos:notation
RIV/00216208:11130/11:7091!RIV12-MZ0-11130___
n11:predkladatel
n12:orjk%3A11130
n3:aktivita
n20:Z n20:P
n3:aktivity
P(NS10489), Z(MSM0021620812)
n3:cisloPeriodika
1
n3:dodaniDat
n17:2012
n3:domaciTvurceVysledku
n9:3785769 n9:2780089 n9:6258883 n9:5285593 n9:1891871 n9:1110047 n9:5730244
n3:druhVysledku
n6:J
n3:duvernostUdaju
n19:S
n3:entitaPredkladatele
n8:predkladatel
n3:idSjednocenehoVysledku
198676
n3:idVysledku
RIV/00216208:11130/11:7091
n3:jazykVysledku
n4:eng
n3:klicovaSlova
Th17 lymphocytes; hyper-IgE; chronic granulomatous disease; candida infections; hyper-ige syndrome; t(h)17 cells; dendritic cells; interleukin-17; responses; pathway; card9; il-23; il-17; differentiation
n3:klicoveSlovo
n7:il-17 n7:il-23 n7:candida%20infections n7:t%28h%2917%20cells n7:Th17%20lymphocytes n7:responses n7:card9 n7:chronic%20granulomatous%20disease n7:pathway n7:dendritic%20cells n7:interleukin-17 n7:hyper-IgE n7:hyper-ige%20syndrome n7:differentiation
n3:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n3:kontrolniKodProRIV
[06A8A937DC95]
n3:nazevZdroje
Clinical and Experimental Immunology
n3:obor
n21:EC
n3:pocetDomacichTvurcuVysledku
7
n3:pocetTvurcuVysledku
7
n3:projekt
n10:NS10489
n3:rokUplatneniVysledku
n17:2011
n3:svazekPeriodika
166
n3:tvurceVysledku
Rožková, Daniela Sedláček, Petr Lašťovička, Jan Šedivá, Anna Špíšek, Radek Poloučková, Andrea Horváth, Rudolf
n3:wos
000294913700003
n3:zamer
n15:MSM0021620812
s:issn
0009-9104
s:numberOfPages
8
n16:organizacniJednotka
11130