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231226s2023 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2023.109793
|2 doi
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|a pubmed24n1209.xml
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|a (DE-627)NLM362728925
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|a (NLM)37776967
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|a (PII)S1521-6616(23)00556-9
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Vladyka, Ondrej
|e verfasserin
|4 aut
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|a Th1/interferon-γ bias in 22q11.2 deletion syndrome is driven by memory T cells and exacerbated by IL-7
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|c 2023
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
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|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 06.11.2023
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|a Date Revised 06.11.2023
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.
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|a 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
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Exhaustion
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|a IFN-γ
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|a IL-7
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|a Immunodeficiency
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|a RNA-seq
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|a Spectral cytometry
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|a thymus
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|a Interferon-gamma
|2 NLM
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|a 82115-62-6
|2 NLM
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| 650 |
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|a Interleukin-7
|2 NLM
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| 650 |
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|a Cytokines
|2 NLM
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| 700 |
1 |
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|a Vrabcova, Petra
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Reiterova, Michaela
|e verfasserin
|4 aut
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| 700 |
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|a Parackova, Zuzana
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Haesler, Robert
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Sediva, Anna
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Kalina, Tomas
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Klocperk, Adam
|e verfasserin
|4 aut
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| 773 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 256(2023) vom: 05. Nov., Seite 109793
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
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|g volume:256
|g year:2023
|g day:05
|g month:11
|g pages:109793
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|u http://dx.doi.org/10.1016/j.clim.2023.109793
|3 Volltext
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