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mljgoums 2018, 12(2): 38-43 |
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Heydarifard Z, Tabarraei A, Abdollahi N, Moradi A, Khanjari Y. Evaluation of CCR5Δ32 Polymorphism in Patients with Systemic Lupus Erythematosus and Healthy Individuals. mljgoums 2018; 12 (2) :38-43
URL: http://mlj.goums.ac.ir/article-1-1073-en.html
URL: http://mlj.goums.ac.ir/article-1-1073-en.html
1- Research Committee Student, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran
2- Infectious Disease Research Center, Golestan University of Medical Sciences, Gorgan, Iran ,Tabarraei@goums.ac.ir
3- Bone, Joint and Connective Tissue Research Center, Golestan University of Medical Sciences, Gorgan, Iran
4- Infectious Disease Research Center, Golestan University of Medical Sciences, Gorgan, Iran
2- Infectious Disease Research Center, Golestan University of Medical Sciences, Gorgan, Iran ,
3- Bone, Joint and Connective Tissue Research Center, Golestan University of Medical Sciences, Gorgan, Iran
4- Infectious Disease Research Center, Golestan University of Medical Sciences, Gorgan, Iran
Abstract: (12004 Views)
ABSTRACT
Background and Objectives: C-C chemokine receptor type 5 (CCR5) is a chemokine receptor expressed at high levels on the surface of T-cells. A 32-bp deletion in the coding region of the CCR5 (CCR5Δ32) leads to production of an incomplete protein that is not expressed on the cell surface. CCR5Δ32 may be involved in development of autoimmune disease, such as systemic lupus erythematosus. We investigated frequency of the CCR5Δ32 polymorphism in SLE patients and healthy controls, and evaluated the relationship between the CCR5Δ32 polymorphism and susceptibility to SLE in Golestan Province, Iran.
Methods: Whole blood samples were taken from 80 SLE patients admitted to Shahid Sayyad Shirazi hospital and 80 healthy controls (from a blood bank) in the Golestan Province, in 2016. Baseline clinical and laboratorial characteristics were evaluated regarding the CCR5Δ32 genotypes. The CCR5Δ32 polymorphism was determined from genomic DNA by polymerase chain reaction.
Result: Genotype frequencies of both groups were in the Hardy-Weinberg equilibrium. The frequencies of the CCR5 and the CCR5Δ32 alleles were 98.13% and 1.88% among the patients, and 98.75% and 1.25% among the controls, respectively. Homozygote CCR5Δ32 was not observed in the subjects. The frequency of heterozygous Δ32 was 3.8% and 2.5% among the SLE patients and controls, respectively (P-value>0.05). There was no significant association between the CCR5 status and clinical signs of SLE (P>0.05).
Conclusion: Our data suggest that the CCR5Δ32 polymorphism has no correlation with SLE in our study population. In addition, the frequency of the Δ32 polymorphism in SLE patients and controls does not follow the Hardy-Weinberg equilibrium
Keywords: CCR5, Homozygote CCR5Δ32, Heterozygote CCR5Δ32, CCR5Δ32 allele, SLE.
Background and Objectives: C-C chemokine receptor type 5 (CCR5) is a chemokine receptor expressed at high levels on the surface of T-cells. A 32-bp deletion in the coding region of the CCR5 (CCR5Δ32) leads to production of an incomplete protein that is not expressed on the cell surface. CCR5Δ32 may be involved in development of autoimmune disease, such as systemic lupus erythematosus. We investigated frequency of the CCR5Δ32 polymorphism in SLE patients and healthy controls, and evaluated the relationship between the CCR5Δ32 polymorphism and susceptibility to SLE in Golestan Province, Iran.
Methods: Whole blood samples were taken from 80 SLE patients admitted to Shahid Sayyad Shirazi hospital and 80 healthy controls (from a blood bank) in the Golestan Province, in 2016. Baseline clinical and laboratorial characteristics were evaluated regarding the CCR5Δ32 genotypes. The CCR5Δ32 polymorphism was determined from genomic DNA by polymerase chain reaction.
Result: Genotype frequencies of both groups were in the Hardy-Weinberg equilibrium. The frequencies of the CCR5 and the CCR5Δ32 alleles were 98.13% and 1.88% among the patients, and 98.75% and 1.25% among the controls, respectively. Homozygote CCR5Δ32 was not observed in the subjects. The frequency of heterozygous Δ32 was 3.8% and 2.5% among the SLE patients and controls, respectively (P-value>0.05). There was no significant association between the CCR5 status and clinical signs of SLE (P>0.05).
Conclusion: Our data suggest that the CCR5Δ32 polymorphism has no correlation with SLE in our study population. In addition, the frequency of the Δ32 polymorphism in SLE patients and controls does not follow the Hardy-Weinberg equilibrium
Keywords: CCR5, Homozygote CCR5Δ32, Heterozygote CCR5Δ32, CCR5Δ32 allele, SLE.
Research Article: Original Paper |
Received: 2018/04/29 | Accepted: 2018/04/29 | Published: 2018/04/29 | ePublished: 2018/04/29
Received: 2018/04/29 | Accepted: 2018/04/29 | Published: 2018/04/29 | ePublished: 2018/04/29
References
1. Blanpain C, Doranz BJ, Bondue A, Govaerts C, De Leener A, Vassart G, et al. The core domain of chemokines binds CCR5 extracellular domains while their amino terminus interacts with the transmembrane helix bundle. Journal of Biological Chemistry. 2003; 278(7): 5179-87. [DOI:10.1074/jbc.M205684200]
2. Gade-Andavolu R, Comings DE, MacMurray J, Rostamkhani M, Cheng LS-C, Tourtellotte WW, et al. Association of CCR5 Δ32 deletion with early death in multiple sclerosis. Genetics in Medicine. 2004; 6(3): 126-31. DOI:10.109701.GIM.0000127274.45301.54.
3. Salem AH, Farid E, Fadel R, Abu-Hijleh M, Almawi W, Han K, et al. Distribution of four HIV type 1-resistance polymorphisms (CCR5-Δ 32, CCR5-m303, CCR2-64I, and SDF1-3′ A) in the Bahraini population. AIDS research and human retroviruses. 2009; 25(10): 973-7. doi: 10.1089/aid.2009.0066. [DOI:10.1089/aid.2009.0066]
4. Grimaldi R, Shindo N, Acosta A, Dourado I, Brites C, de Melo Carvalho O, et al. Prevalence of the CCR5Δ32 mutation in Brazilian populations and cell susceptibility to HIV-1 infection. Human genetics. 2002; 111(1): 102-4. [DOI:10.1007/s00439-002-0747-x]
5. Gharagozloo M, Doroudchi M, Farjadian S, Pezeshki AM, Ghaderi A. The frequency of CCR5Δ32 and CCR2-64I in southern Iranian normal population. Immunology letters. 2005; 96(2): 277-81. [DOI:10.1016/j.imlet.2004.09.007]
6. Adler G, Valjevac A, Skonieczna-Żydecka K, Mackic-Djurovic M, Parczewski M, Urbańska A, et al. Frequency of CCR5Δ32 allele in healthy Bosniak population. Bosnian Journal of Basic Medical Sciences. 2014; 14(3): 150-4. [DOI:10.17305/bjbms.2014.3.102]
7. Lopalco L. CCR5: from natural resistance to a new anti-HIV strategy. Viruses. 2010; 2(2): 574-600. [DOI:10.3390/v2020574]
8. Martens HA, Gross S, van der STEEGE G, Brouwer E, Berden JH, de SEVAUX R, et al. Lack of association of CC chemokine receptor 5 Δ32 deletion status with rheumatoid arthritis, systemic lupus erythematosus, lupus nephritis, and disease severity. The Journal of rheumatology. 2010; 37(11): 2226-31. [DOI:10.3899/jrheum.091468]
9. Longo D, Fauci A, Kasper D, Hauser S, Jameson J, Loscalzo J. Harrison's Principles of Internal Medicine. 18th ed. McGraw-Hill Education; 2011.
10. Zhang J, Dou Y, Zhong Z, Su J, Xu D, Tang F, et al. Clinical characteristics and therapy exploration of active human cytomegalovirus infection in 105 lupus patients. Lupus. 2014;23(9):889-97. doi: 10.1177/0961203314532560. [DOI:10.1177/0961203314532560]
11. Skare TL, Dagostini JS, Zanardi PI, Nisihara RM. Infections and systemic lupus erythematosus. Einstein (São Paulo). 2016; 14(1): 47-51. doi: 10.1007/s10096-014-2098-7. [DOI:10.1007/s10096-014-2098-7]
12. Chen J, Zhang H, Chen P, Lin Q, Zhu X, Zhang L, et al. Correlation between systemic lupus erythematosus and cytomegalovirus infection detected by different methods. Clinical rheumatology. 2015; 34(4): 691-8. doi: 10.1007/s10067-015-2868-3. [DOI:10.1007/s10067-015-2868-3]
13. Zakeri Z, Shakiba M, Narouie B, Mladkova N, Ghasemi-Rad M, Khosravi A. Prevalence of depression and depressive symptoms in patients with systemic lupus erythematosus: Iranian experience. Rheumatology international. 2012; 32(5):1179-87. doi: 1007/s00296-010-1791-9.
14. Baltus THL, Kallaur AP, Lozovoy MAB, Morimoto HK, Delongui F, Alfieri DF, et al. CCR5Δ32 (rs333) polymorphism is associated with the susceptibility to systemic lupus erythematosus in female Brazilian patients. Rheumatology international. 2016; 36(1): 7-15. doi: 10.1007/s00296-015-3308-z. [DOI:10.1007/s00296-015-3308-z]
15. Tan X-h, Zhang J-y, Di C-h, Hu A-r, Yang L, Qu S, et al. Distribution of CCR5-Δ32, CCR5m303A, CCR2-64I and SDF1-3′ A in HIV-1 infected and uninfected high-risk Uighurs in Xinjiang, China. Infection, Genetics and Evolution. 2010; 10(2): 268-72. doi: 10.1016/j.meegid.2009.11.015. [DOI:10.1016/j.meegid.2009.11.015]
16. Arababadi MK, Pourfathollah AA, Jafarzadeh A, Hassanshahi G, Mohit M, Hajghani M, et al. Peripheral blood CD8+ T cells CCR5 expression and its Δ32 mutation in Iranian patients with occult hepatitis B infections. Lab Medicine. 2010; 41(4): 226-30. [DOI:10.1309/LMVUKWROX0EBQR01]
17. Omrani D, Bagheri M. Frequency of CCR5? 32 Variant in North-West of Iran. Journal of Sciences, Islamic Republic of Iran. 2009; 20(2): 105-110.
18. Aguilar F, Nú-ez-Roldán A, Torres B, Wichmann I, Sánchez-Román J, González-Escribano MF. Chemokine receptor CCR2/CCR5 polymorphism in Spanish patients with systemic lupus erythematosus. The Journal of rheumatology. 2003; 30(8): 1770-4.
19. Mamtani M, Rovin B, Brey R, Camargo JF, Kulkarni H, Herrera M, et al. CCL3L1 gene-containing segmental duplications and polymorphisms in CCR5 affect risk of systemic lupus erythematosus. Annals of the rheumatic diseases. 2008; 67(8): 1076-83. doi: 10.1136/ard.2007.078048. [DOI:10.1136/ard.2007.078048]
20. Carvalho C, Calvisi S, Leal B, Bettencourt A, Marinho A, Almeida I, et al. CCR5‐Delta32: implications in SLE development. International journal of immunogenetics. 2014; 41(3): 236-41. doi: 10.1111/iji.12094. [DOI:10.1111/iji.12094]
21. Silva-Carvalho WHV, de Moura RR, Coelho AVC, Crovella S, Guimarães RL. Frequency of the CCR5-delta32 allele in Brazilian populations: A systematic literature review and meta-analysis. Infection, Genetics and Evolution. 2016; 43: 101-7. doi: 10.1016/j.meegid.2016.05.024. [DOI:10.1016/j.meegid.2016.05.024]
22. Rahimi H, Farajollahi MM, Hosseini A. Distribution of the mutated delta 32 allele of CCR5 co-receptor gene in Iranian population. Medical journal of the Islamic Republic of Iran. 2014; 28:140.
23. Ghorban K, Dadmanesh M, Hassanshahi G, Momeni M, Zare-Bidaki M, Arababadi MK, et al. Is the CCR5 Δ 32 mutation associated with immune system-related diseases? Inflammation. 2013; 36(3): 633-42. [DOI:10.1007/s10753-012-9585-8]
24. Hoffman RW. T cells in the pathogenesis of systemic lupus erythematosus. Clinical Immunology. 2004; 113(1): 4-13. [DOI:10.1016/j.clim.2004.05.001]
25. Arababadi MK, Naghavi N, Hassanshahi G, Mahmoodi M. Is CCR5-Δ32 mutation associated with diabetic nephropathy in type 2 diabetes? Annals of Saudi medicine. 2009; 29(5): 413. doi: 10.4103/0256-4947.55177. [DOI:10.4103/0256-4947.55177]
26. Dobaczewski M, Xia Y, Bujak M, Gonzalez-Quesada C, Frangogiannis NG. CCR5 signaling suppresses inflammation and reduces adverse remodeling of the infarcted heart, mediating recruitment of regulatory T cells. The American journal of pathology. 2010; 176(5): 2177-87. doi: 10.2353/ajpath.2010.090759. [DOI:10.2353/ajpath.2010.090759]
27. Li Y-m, Chen Z-q, Yao X, Yang A-z, Li A-s, Liu D-m, et al. mRNA expression of chemokine receptors on peripheral blood mononuclear cells and correlation with clinical features in systemic lupus erythematosus patients. Chinese Medical Sciences Journal. 2010; 25(3): 162-8. [DOI:10.1016/S1001-9294(10)60042-9]
28. Al-Saleh J, el-Eissawy S. The role of T helper cell subsets in pathogenesis of Systemic Lupus Erythematosus and their relation to disease activity. The Egyptian journal of immunology/Egyptian Association of Immunologists. 2005; 13(2): 41-8.
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