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:: Volume 21, Issue 3 (10-2019) ::
J Gorgan Univ Med Sci 2019, 21(3): 88-93 Back to browse issues page
Association of rs2232365 polymorphism in promoter of FOXP3 gene with the incidence of rheumatoid arthritis in Iranian population
Nasimeh Mahmoodi1 , Maryam Peymani * 2, Seyed Morteza Javadirad3
1- M.Sc in Biology, Department of Biology, Faculty of Basic Sciences, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran
2- Assistance Professor, Department of Biology, Faculty of Basic Sciences, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran , peymani62_m@yahoo.com
3- Assistance Professor, Department of Biology, Faculty of Sciences, University of Isfahan, Isfahan, Iran
Abstract:   (10810 Views)
Background and Objective: Rheumatoid arthritis (RA) is the most common systemic inflammatory disease. The FOXP3 gene is an agent that activates during the course of the disease and accumulates in the sinus arthritis of the inflamed joints, resulting in persistent inflammation and ultimately tissue damage. Regarding the role of polymorphism in promoter regions in gene expression, this study was conducted to determine the association of rs2232365 polymorphism in promoter of FOXP3 gene with the incidence of rheumatoid arthritis in Iranian population.
Methods: In this case-control study, in order to investigate the relationship between FOXP3 gene rs2232365 polymorphism and rheumatoid arthritis, 77 patients and 67 healthy subjects were evaluated. The genotype of individuals for polymorphism rs2232365 was determined by PCR-RFLP method.
Results: The highest genotypic frequency was related to CC genotype with 89% frequency in two healthy and diseased populations and no difference was observed in genotypic and allelic abundance in healthy and patient populations. Different genotypes of this polymorphism did not have a significant relation with the risk of RA, while it had a significant correlation with the level of CCP factor and CC genotype was associated with the progression of RA disease by increasing the level of CCP (P<0.05).
Conclusion: This study showed that there is no correlation between polymorphism rs2232365 in promoter of FOXP3 gene with Rheumatoid arthritis in Iranian population.
Keywords: Rheumatoid arthritis, Polymorphism, rs2232365, FOXP3 gene, Iran
Full-Text [PDF 212 kb]   (16631 Downloads)    
Type of Study: Original Articles | Subject: Internal Medicine
References
1. Dowman B, Campbell RM, Zgaga L, Adeloye D, Chan KY. Estimating the burden of rheumatoid arthritis in Africa: A systematic analysis. J Glob Health. 2012 Dec; 2(2): 020406. doi: 10.7189/jogh.02.020406
2. Goldblatt F, Isenberg DA. New therapies for rheumatoid arthritis. Clin Exp Immunol. 2005 May; 140(2): 195-204. doi: 10.1111/j.1365-2249.2005.02744.x
3. Edwards CJ, Cooper C. Early environmental factors and rheumatoid arthritis. Clin Exp Immunol. 2006 Jan; 143(1): 1-5. doi: 10.1111/j.1365-2249.2005.02940.x
4. Molina V, Shoenfeld Y. Infection, vaccines and other environmental triggers of autoimmunity. Autoimmunity. 2005 May; 38(3): 235-45. doi: 10.1080/08916930500050277
5. Shen H, Goodall JC, Hill Gaston JS. Frequency and phenotype of peripheral blood Th17 cells in ankylosing spondylitis and rheumatoid arthritis. Arthritis Rheum. 2009 Jun; 60(6): 1647-56. doi: 10.1002/art.24568
6. Waite JC, Skokos D. Th17 response and inflammatory autoimmune diseases. Int J Inflam. Volume 2012, Article ID 819467. http://dx.doi.org/10.1155/2012/819467
7. McGuirk P, Mills KH. Pathogen-specific regulatory T cells provoke a shift in the Th1/Th2 paradigm in immunity to infectious diseases. Trends Immunol. 2002 Sep; 23(9): 450-55.
8. Shevach EM. CD4+ CD25+ suppressor T cells: more questions than answers. Nat Rev Immunol. 2002 Jun; 2(6): 389-400. doi: 10.1038/nri821
9. Williams LM, Rudensky AY. Maintenance of the Foxp3-dependent developmental program in mature regulatory T cells requires continued expression of Foxp3. Nat Immunol. 2007 Mar; 8(3): 277-84. doi: 10.1038/ni1437
10. Pillai V, Karandikar NJ. Human regulatory T cells: a unique, stable thymic subset or a reversible peripheral state of differentiation? Immunol Lett. 2007 Nov; 114(1): 9-15. doi: 10.1016/j.imlet.2007.08.012
11. Lozano T, Casares N, Lasarte JJ. Searching for the Achilles Heel of FOXP3. Front Oncol. 2013 Dec; 3: 294. doi: 10.3389/fonc.2013.00294
12. Paradowska-Gorycka A, Jurkowska M, Felis-Giemza A, Romanowska-Próchnicka K, Manczak M, Maslinski S, et al. Genetic polymorphisms of Foxp3 in patients with rheumatoid arthritis. J Rheumatol. 2015 Feb; 42(2): 170-80. doi: 10.3899/jrheum.131381
13. Naderi-Mahabadi F, Zarei S, Fatemi R, Kamali K, Pahlavanzadeh Z, Jeddi-Tehrani M, et al. Association study of forkhead box P3 gene polymorphisms with unexplained recurrent spontaneous abortion. J Reprod Immunol. 2015 Aug; 110: 48-53. doi: 10.1016/j.jri.2015.04.001
14. Hashemi V, Farrokhi AS, Tanomand A, Babaloo Z, Hojjat-Farsangi M, Anvari E, et al. Polymorphism of Foxp3 gene affects the frequency of regulatory T cells and disease activity in patients with rheumatoid arthritis in Iranian population. Immunol Lett. 2018 Dec; 204: 16-22. doi: 10.1016/j.imlet.2018.10.001
15. Miller SA, Dykes DD, Polesky HF. A simple salting out procedure for extracting DNA from human nucleated cells. Nucleic Acids Res. 1988 Feb; 16(3): 1215.
16. Lin SC, Chen KH, Lin CH, Kuo CC, Ling QD, Chan CH. The quantitative analysis of peripheral blood FOXP3-expressing T cells in systemic lupus erythematosus and rheumatoid arthritis patients. Eur J Clin Invest. 2007 Dec; 37(12): 987-96. doi: 10.1111/j.1365-2362.2007.01882.x
17. Rahnama R, Mansouri R, Valizadeh H, Rahimdel A, Eslami G. [Investigating Prevalence of FOXP3 Gene Polymorphism in Multiple Sclerosis]. J Shahid Sadoughi Uni Med Sci. 2015; 22(6): 1604-11. [Article in Persian]
18. Bahadivand Chegini H, Pourgheysari B, Pourahmadiyan A, Kazemi S, Shirzad H, Mosavi M, et al. [Association between rs56066773 and rs56232250 polymorphisms of FOXP3 gene in target site of microRNA with rheumatoid arthritis in patients referred to Emam Ali clinic of Shahrekord]. J Shahrekord Univ Med Sci. 2016; 18(1): 9-17. [Article in Persian]
19. Mahdavi R, Jamali M, Rostami M, Safa A, Jafarzadeh A, Naseri M. [FOXP3 polymorphism rs2232365 and its association with multiple sclerosis susceptibility]. Tehran Univ Med J. 2016; 74(6): 425-32. [Article in Persian]
20. Jafarzadeh A, Mahdavi R, Jamali M, Hajghani H, Nemati M, Ebrahimi HA. Increased Concentrations of Interleukin-33 in the Serum and Cerebrospinal Fluid of Patients with Multiple Sclerosis. Oman Med J. 2016 Jan; 31(1): 40-45. doi: 10.5001/omj.2016.08
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Mahmoodi N, Peymani M, Javadirad S M. Association of rs2232365 polymorphism in promoter of FOXP3 gene with the incidence of rheumatoid arthritis in Iranian population. J Gorgan Univ Med Sci 2019; 21 (3) :88-93
URL: http://goums.ac.ir/journal/article-1-3337-en.html
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Volume 21, Issue 3 (10-2019) Back to browse issues page
مجله دانشگاه علوم پزشکی گرگان Journal of Gorgan University of Medical Sciences
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