Th1/interferon-γ bias in 22q11.2 deletion syndrome is driven by memory T cells and exacerbated by IL-7
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F23%3A10470118" target="_blank" >RIV/00216208:11130/23:10470118 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00064203:_____/23:10470118
Výsledek na webu
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=aAC5mwKfxB" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=aAC5mwKfxB</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.clim.2023.109793" target="_blank" >10.1016/j.clim.2023.109793</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Th1/interferon-γ bias in 22q11.2 deletion syndrome is driven by memory T cells and exacerbated by IL-7
Popis výsledku v původním jazyce
The aim of this study was to investigate the impact of thymic dysplasia on the phenotypic and functional characteristics of T cells in patients with 22q11.2 deletion syndrome, including T-cell phenotype, transcriptional profile, cytokine production, as well as the possibility of utilizing IL-7 to recover their numbers and function. We found a strong bias towards Th1 response in pediatric and young adult 22q11.2DS patients, expansion of CXCR5(+) follicular helper cells and CXCR3(+)CCR6(-) Th1 cells, increased production of cytokines IFN-γ, IL-10, IL-2, IL-21 and TNF-α. This Th1 skew was primarily driven by expanded terminally differentiated T cells. IL-7 further reduced naive T cells, increased cytokine production and caused an upregulation of exhaustion markers. Thus, Th1 bias in T cell populations persists from infancy into adolescence and is accompanied by accelerated maturation of T cells into memory stages. This phenotype is exacerbated by IL-7 which causes further decrease in naïve T cells in vitro.
Název v anglickém jazyce
Th1/interferon-γ bias in 22q11.2 deletion syndrome is driven by memory T cells and exacerbated by IL-7
Popis výsledku anglicky
The aim of this study was to investigate the impact of thymic dysplasia on the phenotypic and functional characteristics of T cells in patients with 22q11.2 deletion syndrome, including T-cell phenotype, transcriptional profile, cytokine production, as well as the possibility of utilizing IL-7 to recover their numbers and function. We found a strong bias towards Th1 response in pediatric and young adult 22q11.2DS patients, expansion of CXCR5(+) follicular helper cells and CXCR3(+)CCR6(-) Th1 cells, increased production of cytokines IFN-γ, IL-10, IL-2, IL-21 and TNF-α. This Th1 skew was primarily driven by expanded terminally differentiated T cells. IL-7 further reduced naive T cells, increased cytokine production and caused an upregulation of exhaustion markers. Thus, Th1 bias in T cell populations persists from infancy into adolescence and is accompanied by accelerated maturation of T cells into memory stages. This phenotype is exacerbated by IL-7 which causes further decrease in naïve T cells in vitro.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30102 - Immunology
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Ostatní
Rok uplatnění
2023
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Clinical Immunology
ISSN
1521-6616
e-ISSN
1521-7035
Svazek periodika
256
Číslo periodika v rámci svazku
November
Stát vydavatele periodika
US - Spojené státy americké
Počet stran výsledku
9
Strana od-do
109793
Kód UT WoS článku
001100663700001
EID výsledku v databázi Scopus
2-s2.0-85173948421