Immunologic Abnormalities in β-Thalassemia

β-thalassemia is a hereditary hemolytic anemia associated with a decrease or complete lack of synthesis of β-globin chains as a result of inheriting the mutant gene. Currently there are more than 100 varieties of hemoglobin gene mutations, which can lead to β-thalassemia. In the world there are 60-70 thousand patients with major form of this genetic anomaly. The basic treatment for β-thalassemia is a lifelong hemotransfusion therapy (hypertransfusion regime) that requires to maintain normal levels of hemoglobin and to suppress enhanced but ineffective erythropoiesis. However, volumetric and multiple transfusions inevitably lead to alloimmunization, accumulation of iron in the tissues and are associated with increased risk for transmitted infections [1].