Imbalance of stem-like and effector T cell states in children with early type 1 diabetes across conventional and regulatory subsets

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F25%3A00644126" target="_blank" >RIV/68378050:_____/25:00644126 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11130/25:10506516 RIV/00216208:11310/25:10506516 RIV/00064203:_____/25:10506516

Výsledek na webu

<a href="https://doi.org/10.1038/s41467-025-66459-4" target="_blank" >https://doi.org/10.1038/s41467-025-66459-4</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/s41467-025-66459-4" target="_blank" >10.1038/s41467-025-66459-4</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Imbalance of stem-like and effector T cell states in children with early type 1 diabetes across conventional and regulatory subsets

Popis výsledku v původním jazyce

Type 1 diabetes (T1D) is an autoimmune disease caused by the loss of self-tolerance toward insulin-producing pancreatic beta-cells. Its etiology remains incompletely understood but involves dysregulated T cell responses. Here, we perform single-cell transcriptomic analysis of peripheral blood T cells from children newly diagnosed with T1D, the same children after one year, and healthy donors. We observe that children with diabetes show diminished effector and cytotoxic programs and enhanced stemness-associated gene signature across diverse T cell subsets, especially at diagnosis. In parallel, we detect signs of impaired regulatory capacity in regulatory T cells and regulatory TR3-56 cells. These findings are supported by flow cytometry analysis of the same cohort and reanalysis of publicly available datasets. Overall, our results suggest that T1D is associated with impaired T cell effector differentiation and regulatory T cell dysfunction, both of which may contribute to immune imbalance and loss of self-tolerance.

Název v anglickém jazyce

Imbalance of stem-like and effector T cell states in children with early type 1 diabetes across conventional and regulatory subsets

Popis výsledku anglicky

Type 1 diabetes (T1D) is an autoimmune disease caused by the loss of self-tolerance toward insulin-producing pancreatic beta-cells. Its etiology remains incompletely understood but involves dysregulated T cell responses. Here, we perform single-cell transcriptomic analysis of peripheral blood T cells from children newly diagnosed with T1D, the same children after one year, and healthy donors. We observe that children with diabetes show diminished effector and cytotoxic programs and enhanced stemness-associated gene signature across diverse T cell subsets, especially at diagnosis. In parallel, we detect signs of impaired regulatory capacity in regulatory T cells and regulatory TR3-56 cells. These findings are supported by flow cytometry analysis of the same cohort and reanalysis of publicly available datasets. Overall, our results suggest that T1D is associated with impaired T cell effector differentiation and regulatory T cell dysfunction, both of which may contribute to immune imbalance and loss of self-tolerance.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30102 - Immunology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Nature Communications

ISSN

2041-1723

e-ISSN

2041-1723

Svazek periodika

16

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

20

Strana od-do

11301

Kód UT WoS článku

001645378000001

EID výsledku v databázi Scopus

2-s2.0-105025461540