Does Endoplasmic Reticulum (ER) Stress Contribute to T-cell Exhaustion in B-ALL?

Glucose deprivation in T lymphocytes can trigger compensatory metabolic pathways, potentially contributing to T-cell exhaustion. Additionally, it may induce the unfolded protein response (UPR), ultimately resulting in endoplasmic reticulum (ER) stress. To examine the transcriptional profiles of endo...

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Vydané v:Iranian journal of immunology Ročník 22; číslo 2; s. 100
Hlavní autori: Kahrizi, Amir, Akbar, Armin, Najafi, Ahmad, Asgarian-Omran, Hossein, Karami, Hossein, Naderisorki, Mohammad, Karimi, Alireza, Tehrani, Mohsen
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Iran Shiraz Institute for Cancer Research 01.06.2025
Predmet:
CD8 antigen
Cell activation
Endoplasmic reticulum
Gene expression
Lymphocytes
Lymphocytes T
Metabolic pathways
Peripheral blood
Protein folding
ISSN:1735-1383, 1735-367X, 1735-367X
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Shrnutí:Glucose deprivation in T lymphocytes can trigger compensatory metabolic pathways, potentially contributing to T-cell exhaustion. Additionally, it may induce the unfolded protein response (UPR), ultimately resulting in endoplasmic reticulum (ER) stress. To examine the transcriptional profiles of endoplasmic reticulum (ER) stress markers and T-cell exhaustion indicators in CD8+ T lymphocytes isolated from B-ALL patients. Peripheral blood samples were collected from 22 untreated B-ALL patients and 22 healthy controls. Magnetic Activated Cell Sorting (MACS) was used to isolate CD8+ T lymphocytes. The relative gene expression was then assessed using qRT-PCR with primers specific to XBP1, CHOP, GLUT1, and T-bet. The ER stress response was significantly activated in CD8+ T lymphocytes from B-ALL patients, as evidenced by significant increase in both XBP1 and CHOP transcript levels, relative to normal donors. Although GLUT1 mRNA expression was significantly higher than in control groups, T-bet expression showed no significant difference between the two groups. Collectively, our gene expression data suggest ER stress activation in CD8+ T lymphocytes from B-ALL patients. These findings warrant further investigation into ER stress-related signaling pathways and their potential role in promoting T-cell exhaustion in B-ALL.
Bibliografia:ObjectType-Article-1
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ISSN:1735-1383
1735-367X
1735-367X
DOI:10.22034/iji.2025.105453.2949