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Salehi, Eisa, Vodjgani, Mohammad, massoud, Ahmad, Keyhani, Abdolhosein, Rajab, Asadollah, Shafaghi, Behrooz, Gheflati, Zahra, Aboufazeli, Tahereh. (1386). Increased Expression of TRAIL and Its Receptors on Peripheral T-Cells in Type 1 Diabetic Patients. سامانه مدیریت نشریات علمی, 4(4), 197-205.
Eisa Salehi; Mohammad Vodjgani; Ahmad massoud; Abdolhosein Keyhani; Asadollah Rajab; Behrooz Shafaghi; Zahra Gheflati; Tahereh Aboufazeli. "Increased Expression of TRAIL and Its Receptors on Peripheral T-Cells in Type 1 Diabetic Patients". سامانه مدیریت نشریات علمی, 4, 4, 1386, 197-205.
Salehi, Eisa, Vodjgani, Mohammad, massoud, Ahmad, Keyhani, Abdolhosein, Rajab, Asadollah, Shafaghi, Behrooz, Gheflati, Zahra, Aboufazeli, Tahereh. (1386). 'Increased Expression of TRAIL and Its Receptors on Peripheral T-Cells in Type 1 Diabetic Patients', سامانه مدیریت نشریات علمی, 4(4), pp. 197-205.
Salehi, Eisa, Vodjgani, Mohammad, massoud, Ahmad, Keyhani, Abdolhosein, Rajab, Asadollah, Shafaghi, Behrooz, Gheflati, Zahra, Aboufazeli, Tahereh. Increased Expression of TRAIL and Its Receptors on Peripheral T-Cells in Type 1 Diabetic Patients. سامانه مدیریت نشریات علمی, 1386; 4(4): 197-205.

Increased Expression of TRAIL and Its Receptors on Peripheral T-Cells in Type 1 Diabetic Patients

Iranian Journal of Immunology
مقاله 2، دوره 4، شماره 4، اسفند 2007، صفحه 197-205    اصل مقاله (367.98 K)
نوع مقاله: Original Article
نویسندگان
Eisa Salehi1؛ Mohammad Vodjgani* 1؛ Ahmad massoud1؛ Abdolhosein Keyhani1؛ Asadollah Rajab2؛ Behrooz Shafaghi3؛ Zahra Gheflati1؛ Tahereh Aboufazeli1
1Department of Immunology, Tehran University of Medical Sciences
2Iranian Diabetes Society
3Shahid Beheshti University of Medical Sciences, Tehran, Iran
چکیده
Background: Type-I diabetes is an autoimmune inflammatory disease in which pancreatic ß-cells are selectively destroyed by infiltrating cells. TNF-related apoptosis-inducing ligand (TRAIL) is a type-II membrane protein of the TNF superfamily which is expressed in different tissues, including pancreas and lymphocytes. In humans, TRAIL interacts with four membrane receptors. TRAIL-R1 and TRAIL-R2 have cytoplasmic death domains, and can activate both caspases and NFκB pathways. The other two receptors, TRAIL-R3 and TRAIL-R4, are decoy receptors not capable of activating caspase cascade but may activate NF-κB and block apoptosis. As human beta cells are sensitive to TRAIL induced apoptosis, signaling via these molecules is considered to be a probable way of beta cell destruction. These molecules also are important in suppression of autorective T cells and immunoregulation.
Objective: To explore the importance of TRAIL and its receptors at pathogenesis of type-I diabetes, we compared expression of these molecules on T-cells of diabetic patients and healthy controls.
Methods: In this study, expression of TRAIL and its receptors at protein and mRNA levels were studied in freshly isolated peripheral T cells of 55 type I diabetic patients and 50 healthy individuals by flowcytometry, western blot and RT-PCR.
Results: We found that expression of TRAIL and its receptors in peripheral T-cells at both protein and mRNA levels are significantly increased in patients (except for TRAIL-R2 mRNA which was slightly higher in controls) but increase in TRAIL, TRAIL-R3 (2.7% vs. >0.5%) and TRAIL-R4 (2.6% vs. >0.5%) is more considerable. sTRAIL in sera of patients was significantly lower than in controls (p=0.01).
Conclusion: Our results explain resistance of autoreactive T-cells to immunoregulatory mechanisms. Besides, increased expression of TRAIL in autoreactive T-cells may play an important role in beta-cell destruction. Lower level of sTRAIL in diabetic patients may be a reason for hyperactivation of autoreactive T-cells.
کلیدواژه‌ها
Type I diabetes؛ TRAIL؛ TRAIL receptors؛ T-cell
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