Document Type : Original Article
Authors
- Amir Kahrizi 1
- Armin Akbar 1
- Ahmad Najafi 1
- Hossein Asgarian-Omran 1, 2
- Hossein Karami 3, 4
- Mohammad Naderisorki 3, 4
- Alireza Karimi 1
- Mohsen Tehrani 1, 5
1 Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
2 Gastrointestinal Cancer Research Center, Mazandaran University of Medical Sciences, Sari, Iran.
3 Department of Hematology and Oncology, Imam Khomeini Hospital, Mazandaran University of Medical Sciences, Sari, Iran.
4 Thalassemia Research Center (TRC), Hemoglobinopathy Institute, Mazandaran University of Medical Sciences, Sari, Iran.
5 Molecular and Cell-Biology Research Center, Mazandaran University of Medical Sciences, Sari, Iran.
Abstract
Background: 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.
Objectives: 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.
Methods: 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.
Result: 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..
Conclusion: 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.
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