THE ROLE OF Treg CELLS AND FoxP3 EXPRESSION IN IMMUNITY OF β-THALASSEMIA MAJOR AND β-THALASSEMIA TRAIT PATIENTS

There is increased susceptibility to infections in β-thalassemia. Changes in T- and B-lymphocyte subsets and functions, defective chemotaxis, and phagocytosis of neutrophils and macrophages have been described in these patients. Regulatory T cells (Treg cells) play a crucial role in the maintenance of immunological self-tolerance. The FOXP3 gene is specifically expressed on Treg cells. Increased antigenic stimuli due to repeated blood transfusions might change the Treg cells and FOXP3 percentage in β-thalassemia. Immune functions of peripheral blood lymphocytes, percentage of Treg cells (defined as CD4(+)CD25(+)FoxP3(+)) were evaluated in 30 β-thalassemia major, 30 β-thalassemia trait, and 20 healthy children. Percentage of CD4(+)CD45RA(+) cells were increased in β-thalassemia trait compared to both β-thalassemia major and controls, whereas percentage of CD4(+)CD45RO(+) cells were higher in β-thalassemia major and trait patient compared to controls. Percentages of CD4(+)CD25(bright) and CD4(+)CD25(+)FoxP3(+) Treg cells were increased only in β-thalassemia major patients compared to controls (P = .001 and P = .0001, respectively). T lymphocytes express activated phenotype both in β-thalassemia major and trait patients. However, only in β-thalassemia major patients who were exposed to chronic antigenic stimulus as a result of repeated blood transfusions was an increase observed in Treg cells, which might suppress immune activation status.