A wide spectrum of immune abnormalities has been described
by numerous studies involvin β-thalassemic patients with multiple transfusios.
The abnormalities observed to date are both quantitative and functional, and
concern several components of the immune response. More specifically, the
changes in T-lymphocyte subsets include a greater number and activity of suppressor
T-cells (CD8), reduced proliferative capacity, and a number and level of
activity of helper T-cells (CD4) leading to decreased CD4/CD8 ratios, as well
as defective activity of Natural Killer (NK) cells [4–9].
B lympocytes are characterized by increased numbers, high activation, and
impaired differentiation [4,7,9,10]. Impairment of immunoglobulin secretion
accompanied
by
increased levels of IgG, IgM, and IgA, has also been noticed [4,11,12].
Neutrophils and macrophages are associated with defective chemotaxis and
phagocytosis [13–15]. Finally, suppressed functioning
of the complement system, with reduced levels of C3 and C4, has also been
observed [11,12]. These defects have been attributed both to the disease itself
and the applied therapeutic interventions [4].
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