TITLE:
Role of Complement Regulatory Proteins (CD55, CD59, and CD35) on Red Blood Cells of β-Thalassaemia Patients
AUTHORS:
Hend Hanafy Mahmoud, Nawal Mahrous Nasef, Dalia Mahmoud Eldewi, Rasha Kamel Fathy Galal
KEYWORDS:
CD55, CD59, CD35, β-Thalassemia Major
JOURNAL NAME:
Open Journal of Blood Diseases,
Vol.11 No.4,
October
14,
2021
ABSTRACT: Background: β-thalassaemia
(β-Thal) is an inherited chronic
haemolytic anaemia resulting from absent or low level of
synthesis of β-globin chains of
haemoglobin A in erythropoietic cells. The complement system is an important
part of innate immune response that may be implicated in red blood cell (RBC)
lysis. Mammalian cells are provided with surface bound complement regulatory proteins
(MCRPs) that regulate the activation of complement cascade, thus protecting
them from uncontrolled complement-mediated lysis. Objective is to evaluate the
role of complement regulatory proteins (CD55, CD59, and CD35) on red blood
cells, and to explain the pathogenesis of anaemia in β-thalassemia major. Methods: This case-control study
enrolled 74 β thalassemia major patients
who were compared with 40 age and sex matched controls. We performed expression
of CD55, CD59, and CD35 on RBCs using flow cytometry. Results: CD55
levels of β-thalassemia major
patients (79.78% ± 18.54%) were significantly decreased compared to healthy
controls (99.45% ± 0.59%) (P β-thalassemia major patients
(97.76% ± 1.72%) were significantly lower than in the controls (99.75% ±
0.36%) (P β-thalassemia major patients (4.30% ± 4.66%)
than in the control group (19.40% ± 10.90%) (P Conclusion: β-thalassemia major patients suffer from
increased haemolysis and a consequent increase in their demand for blood
transfusion. Complement-mediated haemolysis was shown in our study by decreased
expression of CD55, CD59, and CD35 in β-thalassemia
major patients. This allows complement deposition on RBCs and enhances or
accelerates their lysis.