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 beta-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 beta-thalassemia. Immune functions of peripheral blood lymphocytes, percentage of Treg cells (defined as CD4(+) CD25(+) FoxP3(+)) were evaluated in 30 beta-thalassemia major, 30 beta-thalassemia trait, and 20 healthy children. Percentage of CD4+ CD45RA(+) cells were increased in beta-thalassemia trait compared to both beta-thalassemia major and controls, whereas percentage of CD4(+) CD45RO(+) cells were higher in beta-thalassemia major and trait patient compared to controls. Percentages of CD4(+) CD25(bright) and CD4(+) CD25(+) FoxP3(+) Treg cells were increased only in beta-thalassemia major patients compared to controls (P = .001 and P = .0001, respectively). T lymphocytes express activated phenotype both in beta-thalassemia major and trait patients. However, only in beta-thalassemia