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Premature Senescence of T Lymphocytes From Patients With Β-Thalassemia Major Publisher Pubmed



Gharagozloo M1, 2 ; Bagherpour B1 ; Tahanian M1 ; Oreizy F1 ; Amirghofran Z2 ; Sadeghi HMM3 ; Hourfar H4 ; Moayedi B1
Authors
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Authors Affiliations
  1. 1. Department of Immunology, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
  3. 3. Department of Pharmaceutical Biotechnology, Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. Division of Thalassemia and Hemophilia, Isfahan University of Medical Sciences, Isfahan, Iran

Source: Immunology Letters Published:2009


Abstract

Several researches have demonstrated a suppressed cell mediated immunity in patients with β-thalassemia major. To know whether the premature aging of T cells is involved in abnormalities of cell mediated immunity, the biomarkers of immunosenescence including telomerase activity, apoptosis, and the expression of CD28 and CD95 were evaluated in T lymphocytes from β-thalassemia major patients. The ex vivo spontaneous apoptosis in CD4+ or CD8+ T cells from patients and healthy subjects was assessed by an in situ TdT mediated dUTP-biotin nick end labelling (TUNEL) assay after 24 h incubation in medium. Flow cytometric data revealed that lymphocytes from β-thalassemia patients were resistant to spontaneous apoptosis compared to the normal lymphocytes. Moreover, the percentages of TUNEL+CD4+ or TUNEL+CD8+ T cells from patients were significantly lower than those control cells. Quantitative determination of telomerase activity in resting and activated T cells was performed using the Telomeric Repeat Amplification Protocol (TRAP). The results showed a decreased telomerase activity of activated T cells in patients with thalassemia major compared to that in healthy controls. However, the percentages of CD8+CD28- and CD3+CD95+ T lymphocytes were significantly higher in thalassemia patients, indicating the phenotypes associated with senescent T lymphocytes. These data provide evidences for the occurrence of accelerated aging of T cells in β-thalassemia major; possibly result in abnormal T cell function leading to suppressed cell mediated immunity. Crown Copyright © 2008.