Premature senescence of T
lymphocytes from patients
With β- Thalassemia Major Patients
Introduction
β- Thalassemia is a hereditary anemia
resulting from defects in the production of β- globin chains. The ineffective erythropoiesis in β- thalassemia is due to defective
hemoglobin synthesis; results in increased RBC turnover and severe anemia,
which can be corrected by regular blood transfusions(Rund and
Rachmilewitz;2005).
Repeated blood transfusions and
RBC hemolysis are the major causes of secondary iron overload and oxidative
stress in β- thalassemia
major(Schrier et al;2003)
Many patients with β- thalassemia major require spleenectomy
Because of
hypersplenism and if annual blood transfusion increases
Progressively.
The major complication of spleenectomy
is severe and sometimes overwhelming infection. Because removal of the spleen reduces
the primary immune response to encapsulated organisms(Maria;2006)
The ageing immune system shows a gradual decline in responsiveness to
antigens. Immunosenescent T cells show several characteristics which can be
seen in both in vivo and in vitro models of ageing(Pawelec and Larbi et
al;2008)
There is a block in cell division
and shortening of telomere length. Also there is a selective decrease in
costimulatory receptors; particularly CD28, which is very significant due to
its pivotal role in providing the stimulation required for a full proliferative
T cell response. However, the apoptotic receptor CD95 being up-regulated(Hakim
and Gress;2007 and Grver et al;2007)
Dr. Nada Fathy
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