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Kalantar, Fathollah, Dabbaghmanesh, Mohammad Hossein, Martinuzzi, Emanuela, Moghadami, Mohsen, Amirghofran, Zahra. (1392). Islet Amyloid Polypeptide is not a Target Antigen for CD8+ T-Cells in Type 2 Diabetes. سامانه مدیریت نشریات علمی, 11(1), 1-12.
Fathollah Kalantar; Mohammad Hossein Dabbaghmanesh; Emanuela Martinuzzi; Mohsen Moghadami; Zahra Amirghofran. "Islet Amyloid Polypeptide is not a Target Antigen for CD8+ T-Cells in Type 2 Diabetes". سامانه مدیریت نشریات علمی, 11, 1, 1392, 1-12.
Kalantar, Fathollah, Dabbaghmanesh, Mohammad Hossein, Martinuzzi, Emanuela, Moghadami, Mohsen, Amirghofran, Zahra. (1392). 'Islet Amyloid Polypeptide is not a Target Antigen for CD8+ T-Cells in Type 2 Diabetes', سامانه مدیریت نشریات علمی, 11(1), pp. 1-12.
Kalantar, Fathollah, Dabbaghmanesh, Mohammad Hossein, Martinuzzi, Emanuela, Moghadami, Mohsen, Amirghofran, Zahra. Islet Amyloid Polypeptide is not a Target Antigen for CD8+ T-Cells in Type 2 Diabetes. سامانه مدیریت نشریات علمی, 1392; 11(1): 1-12.

Islet Amyloid Polypeptide is not a Target Antigen for CD8+ T-Cells in Type 2 Diabetes

Iranian Journal of Immunology
مقاله 1، دوره 11، شماره 1، خرداد 2014، صفحه 1-12    اصل مقاله (942.34 K)
نوع مقاله: Original Article
نویسندگان
Fathollah Kalantar1؛ Mohammad Hossein Dabbaghmanesh2؛ Emanuela Martinuzzi3؛ Mohsen Moghadami4؛ Zahra Amirghofran* 1، 5، 6
1Department of Immunology
2Endocrine and Metabolism Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
3Cochin Institute, Paris, France
4HIV/AIDS Research Center
5Autoimmune Disease Research Center
6Medicinal and Natural Products Chemistry Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
چکیده
Background: Type 2 diabetes (T2D) is a chronic metabolic disorder in which beta-cells are destroyed. The islet amyloid polypeptide (IAPP) produced by beta-cells has been reported to influence beta-cell destruction.
Objective: To evaluate if IAPP can act as an autoantigen and therefore, to see if CD8 + T-cells specific for this protein might be present in T2D patients.
Methods: Peripheral blood mononuclear cells (PBMC) were obtained from human leukocyte antigen (HLA)-A2 + T2D patients and non-diabetic healthy subjects. Cells were then screened for peptide recognition using ELISPOT assay for the presence of IFN-γ producing CD8 + T-cells against two HLA Class I-restricted epitopes derived from IAPP (IAPP 5-13 and IAPP9-17) and common viral antigenic minimal epitopes Flu MP 58-66, CMV495–503, EBV280–288 and HIV77–85 as controls.
Results: A total of 36.4% of patients and 56.2% of healthy subjects showed a response against IAPP 5-13 peptide. No significant difference in response against this peptide was noted between the patients and the healthy donors. With respect to peptide IAPP 9-17, although healthy subjects showed a higher mean number of spot forming cells than the patients, the difference was not significant; 36.4% of patients and 37.5% of controls responded to this peptide. The response of healthy subjects to the common viral peptides was stronger than that of the patients, though the result was not significant.
Conclusions: It is unlikely that IAPP would be a target for CD8+ T-cells in diabetic patients; however, the trend observed toward a lower response of T2D patients against IAPP and common viral peptides may imply a decreased immune response in these patients.
کلیدواژه‌ها
CD8-positive T-Lymphocytes؛ ELISPOT؛ Type 2 Diabetes؛ Islet Amyloid Polypeptide
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