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Kahrizi, Amir, Akbar, Armin, Najafi, Ahmad, Asgarian-Omran, Hossein, Karami, Hossein, Naderisorki, Mohammad, Karimi, Alireza, Tehrani, Mohsen. (1404). Does Endoplasmic Reticulum (ER) Stress Contribute to T-cell Exhaustion in B-ALL?. سامانه مدیریت نشریات علمی, 22(2), -. doi: 10.22034/iji.2025.105453.2949
Amir Kahrizi; Armin Akbar; Ahmad Najafi; Hossein Asgarian-Omran; Hossein Karami; Mohammad Naderisorki; Alireza Karimi; Mohsen Tehrani. "Does Endoplasmic Reticulum (ER) Stress Contribute to T-cell Exhaustion in B-ALL?". سامانه مدیریت نشریات علمی, 22, 2, 1404, -. doi: 10.22034/iji.2025.105453.2949
Kahrizi, Amir, Akbar, Armin, Najafi, Ahmad, Asgarian-Omran, Hossein, Karami, Hossein, Naderisorki, Mohammad, Karimi, Alireza, Tehrani, Mohsen. (1404). 'Does Endoplasmic Reticulum (ER) Stress Contribute to T-cell Exhaustion in B-ALL?', سامانه مدیریت نشریات علمی, 22(2), pp. -. doi: 10.22034/iji.2025.105453.2949
Kahrizi, Amir, Akbar, Armin, Najafi, Ahmad, Asgarian-Omran, Hossein, Karami, Hossein, Naderisorki, Mohammad, Karimi, Alireza, Tehrani, Mohsen. Does Endoplasmic Reticulum (ER) Stress Contribute to T-cell Exhaustion in B-ALL?. سامانه مدیریت نشریات علمی, 1404; 22(2): -. doi: 10.22034/iji.2025.105453.2949

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

Iranian Journal of Immunology
دوره 22، شماره 2، شهریور 2025    اصل مقاله (634.04 K)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22034/iji.2025.105453.2949
نویسندگان
Amir Kahrizi1؛ Armin Akbar1؛ Ahmad Najafi1؛ Hossein Asgarian-Omran1، 2؛ Hossein Karami3، 4؛ Mohammad Naderisorki3، 4؛ Alireza Karimi1؛ Mohsen Tehrani* 1، 5
1Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
2Gastrointestinal Cancer Research Center, Mazandaran University of Medical Sciences, Sari, Iran.
3Department of Hematology and Oncology, Imam Khomeini Hospital, Mazandaran University of Medical Sciences, Sari, Iran.
4Thalassemia Research Center (TRC), Hemoglobinopathy Institute, Mazandaran University of Medical Sciences, Sari, Iran.
5Molecular and Cell-Biology Research Center, Mazandaran University of Medical Sciences, Sari, Iran.
چکیده
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.
کلیدواژه‌ها
Acute Lymphoblastic Leukemia؛ CHOP؛ ER Stress؛ T-cell Exhaustion؛ XBP1
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