Najmaddini H, Hassanshahi G, Ostadebrahimi H, Barkhordari H, Mashayekhi H, Nazari M, et al. Overproduction of CXC chemokines CXCL1, CXCL9, CXCL10 and CXCL12 in b-thalassemia major or patients. Ann Saudi Med 2014; 34(2): 122-7.
Patel NA, Unadkat SV, Mehta JP, Yada SB. A study on transfusion transmitted infections (TTIs), transfusion-related complications, and quality of life among the beta-thalassemia major patients in Jamnagar district. Int J Med Sci Public Health 2016; 5(7): 1447-51.
Elsayh KI, Mohammed WS, Zahran AM, Saad K. Leukocytes apoptosis and adipocytokines in children with beta thalassemia major. Clin Exp Med 2016; 16(3): 345-50.
Balkwill FR. The chemokine system and cancer. The J Pathol 2012; 226(2): 148-57.
Pignatti CB, Carnelli V, Caruso V, Dore F, De Mattia D, Di Palma A, et al. Thromboembolic events in beta thalassemia major: an Italian multicenter study. Acta Haematol 1998; 99(2): 76-9.
Öztürk O, Yaylim İ, Aydin M, Yilmaz H, Agachan B, Demiralp E, et al. Increased plasma levels of interleukin-6 and interleukin-8 in β-thalassaemia major. Haematologia 2001; 31(3): 237-44.
Walker EM Jr, Walker SM. Effects of iron overload on the immune system. Ann Clin Lab Sci 2000; 30(4): 354-65.
Dimitriou E, Verhoek M, Altun S, Karabatsos F, Moraitou M, Youssef J, et al. Elevated plasma chemokine CCL18/PARC in β-thalassemia. Blood Cells Mol Dis 2005; 35(3): 328-31.
Gharagozloo M, Karimi M, Amirghofran Z. Double-faced cell-mediated immunity in β-thalassemia major: stimulated phenotype versus suppressed activity. Ann Hematol 2009; 88(1): 21-7.
Ostadebrahimi H, Jamali Z, Nazari M, Bahri M, Farahmandnia Z, Khandany BK, et al. CXC chemokines CXCL1, CXCL9, CXCL10 and CXCL12 are variably expressed in patients with sickle cell disease and carriers: are they predictive tools for disease complications? Clin Lab 2014; 60(1): 99-104.
Sci J Iran Blood Transfus Organ 2019; 15(4): 287-292
Original Article
The evaluation of chemokine-receptor axis CCL-5/CCR-5 in patients with beta thalassemia major
1Faculty of Allied Medical Sciences, Kerman University of Medical Sciences, Kerman, Iran 2Iranshahr University of Medical Sciences, Iranshahr, Iran 3Department of Hematology and Medical Laboratory Sciences, Faculty of Allied Medical Sciences, Kerman University of Medical Sciences, Kerman, Iran 4Molecular Medicine Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
Abstract Background and Objectives
Immune abnormalities are the fourth leading cause of death in thalassemia major patients. These patients are affected by stimulating chronic immunosuppression and immune deficiency following repeated blood transfusions and iron overload. Considering the role of chemokine network in immunosuppression, we examined the role of CCL-5 chemokine and its receptor CCR-5 in β-Thalassemia major patients.
Materials and Methods
In the present case/control study, 45 β-thalassemia patients having referred to Kerman Special Health Center and 45 healthy subjects as controls participated. For the expression of CCR-5 and CCL5 receptor expression, flow cytometry and ELISA were used, respectively. After the tests, T-test and SPSS software version 22 were used for analysis and p < 0.05 was considered as a significant difference.
Results
Our results indicated that both CCR5 and CCL-5 were induced in β-thalassemia patients compared to the control (p < 0.05).
Conclusions
This study showed the increase of CCL5/CCR5-receptor chemokine-centered axis in patients with thalassemia major compared with healthy subjects and similarly the very increase in patients with spleen compared with those without. Due to the fact that a study on this chemokine network has not been done so far, it is necessary to repeat this study with more samples and to carefully examine the role of the spleen.
Correspondence: Hassan Shahi Gh.H., PhD of Hematology & Blood Banking. Molecular Medicine Research Center, Rafsanjan University of Medical Sciences.
P.O.Box: 7717933777, Rafsanjan, Iran. Tel: (+9834) 31315203 ; Fax: (+9834) 34280097
E-mail: ghassanshahi@gmail.com