Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0039730 (thalassemia)
 10,305 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several researches have demonstrated a suppressed cell mediated immunity in patients with beta-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 beta-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 24h incubation in medium. Flow cytometric data revealed that lymphocytes from beta-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 beta-thalassemia major; possibly result in abnormal T cell function leading to suppressed cell mediated immunity.
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PMID:Premature senescence of T lymphocytes from patients with beta-thalassemia major. 1911 76