CLINICAL IMMUNOLOGY
Expression of CD55, CD59, and CD35 on red blood cells of β-thalassaemia patients
Submission date: 2016-06-20
Final revision date: 2016-10-04
Acceptance date: 2016-10-17
Publication date: 2017-05-08
Cent Eur J Immunol 2017;42(1):78-84
KEYWORDS
ABSTRACT
Aim of the study: β-thalassaemia (β-Thal) is considered a severe, progressive haemolytic anaemia, which needs regular blood transfusions for life expectancy. Complement-mediated erythrocyte destruction can cause both intravascular and extravascular haemolysis. Complement regulatory proteins protect cells from such effects of the complement system. We aimed to perform quantitative analysis of membrane-bound complement regulators, CD55 (decay accelerating factor – DAF), CD35 (complement receptor type 1 – CR1), and CD59 (membrane attack complex inhibitory factor – MACIF) on peripheral red blood cells by flow cytometry.
Material and methods: The present study was carried out on 47 β-thalassemia major (β-TM) patients, 20 β-thalassaemia intermedia (β-TI) patients, and 17 healthy volunteers as control subjects.
Results: CD55 levels of β-TM patients (58.64 ±17.06%) were significantly decreased compared to β-TI patients (83.34 ±13.82%) and healthy controls (88.57 ±11.69%) (p < 0.01). CD59 levels of β-TM patients were not significantly different than β-TI patients and controls, but CD35 levels were significantly lower in the β-TM patients (3.56 ±4.87%) and β-TI patients (12.48 ±9.19%) than in the control group (39.98 ±15.01%) (p < 0.01).
Conclusions: Low levels of CD55 and CD35 in thalassaemia major patients indicates a role for them in the aetiopathogenesis of haemolysis in this disease, and also this defect in a complement system may be responsible for the chronic complications seen in these patients.
Material and methods: The present study was carried out on 47 β-thalassemia major (β-TM) patients, 20 β-thalassaemia intermedia (β-TI) patients, and 17 healthy volunteers as control subjects.
Results: CD55 levels of β-TM patients (58.64 ±17.06%) were significantly decreased compared to β-TI patients (83.34 ±13.82%) and healthy controls (88.57 ±11.69%) (p < 0.01). CD59 levels of β-TM patients were not significantly different than β-TI patients and controls, but CD35 levels were significantly lower in the β-TM patients (3.56 ±4.87%) and β-TI patients (12.48 ±9.19%) than in the control group (39.98 ±15.01%) (p < 0.01).
Conclusions: Low levels of CD55 and CD35 in thalassaemia major patients indicates a role for them in the aetiopathogenesis of haemolysis in this disease, and also this defect in a complement system may be responsible for the chronic complications seen in these patients.
REFERENCES (31)
2.
Rachmilewitz EA, Giardina PJ (2011). How I treat thalassemia Blood 118: 3479-3488.
3.
Galanello R, Origa R (2010) Beta-thalassemia. Orphanet J Rare Dis 5: 11; doi:10.1186/1750-1172-5-11.
4.
Ragab SM, Safan MA, Badr EA (2015): Study of serum haptoglobin level and its relation to erythropoietic activity in Beta thalassemia children. Mediterr J Hematol Infect Dis 7: e2015019.
5.
Ruiz-Argüelles A, Llorente L (2007): The role of complement regulatory proteins (CD55 and CD59) in the pathogenesis of autoimmune hemocytopenias. Autoimmun Rev 6: 155-161.
6.
DeZern AE, Uknis M, Yuan X Mukhina GL (2014): Complement blockade with a C1 esterase inhibitor in paroxysmal nocturnal hemoglobinuria. Exp Hematol 42: 857-861.
7.
Mahajan RC, Narain K, MahantaJ (2011): Anaemia & expression levels of CD35, CD55 & CD59 on red blood cells in Plasmodium falciparum malaria patients from India. Indian.
9.
Johnson JB, Borisevich V, Rocky B, Parks GD (2015): A novel factor activity in Nipah virus inhibits human complement pathways through cleavage of C3b. J Virol 89: 989-998.
10.
Gwamaka M, Fried M, Domingo G, Duffy PE (2011): Early and extensive CD55 loss from red blood cells supports a causal role in malarial anaemia. Malar J 10: 386; doi: 10.1186/1475-2875-10-386.
12.
Sayani FA, Kwiatkowski JL (2015): Increasing prevalence of thalassemia in America: Implications for primary care. Ann Med 47: 592-604.
13.
Xu LH, Fang JP, Weng WJ (2012). Autoimmune hemolytic anemia in patients with -thalassemia major. Pediatr Hematol Oncol. 29: 235-240.
14.
Alegretti AP, Schneider L, Piccoli AK (2012): Diminished expression of complement regulatory proteins on peripheral blood cells from systemic lupus erythematosus patients. Clin Dev Immunol 2012: 725684; doi: 10.1155/2012/725684.
15.
Veerreddy P (2013): Hemoglobinuria misidentified as hematuria: review of discolored urine and paroxysmal nocturnal hemoglobinuria. Clin Med Insights Blood Disord 20: 7-17.
16.
Mahaian RC, Naran K, Mahanta J (2011): Anaemia & expression levels of CD35, CD55 & CD59 on red blood cells in Plasmodium falciparum malaria patients from india. Indian.
17.
Varma S, Varma N, Reddy VV (2012): Detection of paroxysmal nocturnal hemoglobinuria-phenotype in patients with chronic lymphocytic leukemia and multiple myeloma. Indian J Pathol Microbiol 55: 206-210.
18.
Barros MM, Yamamoto M, Figueiredo MS, Cançado R (2009): levels of CD47, CD35, CD55, and CD59 on red blood cells and signal-regulatory protein-alpha, beta on monocytes from patients with warm autoimmune hemolytic anemia. Transfusion 49: 154-160.
19.
Obaid JM, Abo El-Nazar SY, Granem AM El-Hadidi AS (2014): Expression of CD55 on red blood cells of -thalassemia patients. Hemoglobin. 38: 339-344.
20.
Fang C, Miwa T, Shen H Song WC (2007): Complement-dependent enhancement of CD8+ T cell immunity to lymphocytic choriomeningitis virus infection in decay-accelerating factor-deficient mice. J Immunol 179: 3178-3186.
21.
Bao L, Haas M, Minto AW Quigg RJ (2007): Decay-accelerating factor but not CD59 limits experimental immune-complex glomerulonephritis. Lab Invest 87: 357-364.
22.
Rochowiak A, Niemir ZI (2010): The structure and role of CR1 complement receptor in physiology. Pol Merkur Leka 28: 79-83.
23.
Dambal A, Nimbal NV, Kalsad ST, et al. (2015): Paroxysmal nocturnal haemoglobinuria masquerading as malaria: a case report. J Clin Diagn Res 9: OD03-4; doi: 10.7860/JCDR/2015/13465.6329.
24.
Obaid JM, Abo El-Nazar SY, Granem AM, El-Hadidi AS (2015): Compensation of CD55 underexpression on red blood cells of -thalassemia major patients. Hemoglobin 39: 184-189.
25.
Meulenbroek EM, Wouters D, Zeerleder S (2014): Methods for quantitavive detection of antibody-induced complement activation on red blood cells. J Vis Exp 83: e51161.
26.
Berentsen S, Sundic T (2015). Red blood cell destruction in autoimmune hemolytic anemia: role of complement and potential new targets for therapy. Biomed Res Int 2015: 363278; doi: 10.1155/2015/363278.
27.
Cockburn IA, Mackinnon MJ, O’Donnell A, et al. (2004): A human complement receptor 1 polymorphism that reduces Plasmodium falciparum rosetting confers protection against severe malaria. Proc Natl Acad Sci U S A 101: 272-277.
28.
Kumar R, Singh K, Panigrahi I, Agarwal S (2013): Genetic heterogeneity of beta globin mutations among Asian-Indians and importance in genetic counselling and diagnosis. Mediterr J Hematol Infect Dis 5: e2013003; doi: 10.4084/MJHID.2013.003.
29.
Luzzatto L (2016): Recent advances in the pathogenesis and treatment of paroxysmal nocturnal hemoglobinuria. F1000Res. 23; 5. pii: F1000 Faculty Rev-209. doi: 10.12688/f1000research.7288.1.
30.
Khera R, Das N (2009): Complement receptor 1: disease associations and therapeutic implications. Mol Immunol 46: 761-772.
31.
Opi DH, Uyoga S, Orori EN, et al. (2016): Red blood cell complement receptor one level varies with Knops blood group, +thalassaemia and age among Kenyan children. Genes Immun 17: 171-178.
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