Volume 4, Issue 14 (Summer 2018)                   Caspian.J.Neurol.Sci 2018, 4(14): 91-97 | Back to browse issues page

XML Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Alsahebfosoul F, Rahimpourkoldeh S, Eskandari N, Shaygannejad V, Ganjalikhani Hakemi M, Dabiri A, et al . Gene Expression of CD226 and Its Serum Levels in Patients With Multiple Sclerosis. Caspian.J.Neurol.Sci. 2018; 4 (14) :91-97
URL: http://cjns.gums.ac.ir/article-1-233-en.html
1- Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
2- Isfahan Neurosciences Research Center, Alzahra Hospital, Department of Neurology, Isfahan University of Medical Sciences, Isfahan, Iran
3- Department of Immunology, International Campus, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Abstract:   (179 Views)
Background: Recent studies have found some genetic variants as a risk factor for autoimmune diseases such as Multiple Sclerosis (MS). Cluster of Differentiation 226 (CD226) is one of the risk factors for MS. 
Objectives: The present study aimed to evaluate the gene expression of CD226, and its protein serum level in peripheral blood samples of MS patients and healthy individuals.
Materials & Methods: Thirty individuals with MS and 30 healthy individuals, as controls, referred to Kashani Hospital of Isfahan, Iran. CD226 expression at the transcript level and serum protein levels were measured by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assays, respectively. Statistical analyses were performed by Shapiro-Wilk test and nonparametric tests in SPSS. 
Results: The present study showed no significant differences in the gene expression of CD226 (P=0.341). The mean serum protein level of CD226 was not different between the patients and the controls (P=0.978).
Conclusion: Overall, CD226 expression has no diagnostic usefulness in MS at either the transcript or serum level. 
Keywords: Multiple Sclerosis, Demyelinating diseases, Gene expression, Cluster of Differentiation 226 (CD226) antigen
Full-Text [PDF 1342 kb]   (88 Downloads) |   |   Full-Text (HTML)  (7 Views)  
Type of Study: Research | Subject: General
Received: 2018/01/5 | Accepted: 2018/05/23 | Published: 2018/07/1

References
1. Rossi B, Constantin G. Live imaging of immune responses in experimental models of Multiple Sclerosis. Front Immunol. 2016; 7:506. [DOI:10.3389/fimmu.2016.00506] [PMID] [PMCID] [DOI:10.3389/fimmu.2016.00506]
2. Evans C, Beland SG, Kulaga S, Wolfson C, Kingwell E, Marriott J, et al. Incidence and prevalence of Multiple Sclerosis in the Americas: A systematic review. Neuroepidemiology. 2013; 40(3):195-210. [DOI:10.1159/000342779] [PMID] [DOI:10.1159/000342779]
3. Ascherio A, Munger KL, Lunemann JD. The initiation and prevention of Multiple Sclerosis. Nat Rev Neurol. 2012; 8(11):602-12. [DOI:10.1038/nrneurol.2012.198] [PMID] [PMCID] [DOI:10.1038/nrneurol.2012.198]
4. Kamm CP, Uitdehaag BM, Polman CH. Multiple Sclerosis: current knowledge and future outlook. Eur Neurol. 2014; 72(3-4):132-41. [DOI:10.1159/000360528] [PMID] [DOI:10.1159/000360528]
5. Rejali M, Hosseini SM, Kazemi Tabaee MS, Etemadifar M. Assessing the risk factors for Multiple Sclerosis in women of reproductive age suffering the disease in Isfahan province. Int J Prev Med. 2016; 7:58. [DOI:10.4103/2008-7802.178532] [PMID] [PMCID] [DOI:10.4103/2008-7802.178532]
6. O'Gorman C, Lucas R, Taylor B. Environmental risk factors for Multiple Sclerosis: A review with a focus on molecular mechanisms. Int J Mol Sci. 2012; 13(9):11718-52. [DOI:10.3390/ijms130911718] [PMID] [PMCID] [DOI:10.3390/ijms130911718]
7. Olsson T, Barcellos LF, Alfredsson L. Interactions between genetic, lifestyle and environmental risk factors for Multiple Sclerosis. Nat Rev Neurol. 2017; 13(1):25-36. [DOI:10.1038/nrneurol.2016.187] [PMID] [DOI:10.1038/nrneurol.2016.187]
8. Sawcer S, Ban M, Wason J, Dudbridge F. What role for genetics in the prediction of Multiple Sclerosis? Ann Neurol. 2010; 67(1):3-10. [DOI:10.1002/ana.21911] [PMID] [PMCID] [DOI:10.1002/ana.21911]
9. Wang Y, Bos SD, Harbo HF, Thompson WK, Schork AJ, Bettella F, et al. Genetic overlap between Multiple Sclerosis and several cardiovascular disease risk factors. Mult Scler. 2016; 22(14):1783-93. [DOI:10.1177/1352458516635873] [PMID] [PMCID] [DOI:10.1177/1352458516635873]
10. Handunnetthi L, Ramagopalan SV, Ebers GC. Multiple Sclerosis, vitamin D, and HLA-DRB1*15. Neurology. 2010; 74(23):1905-10. [DOI:10.1212/WNL.0b013e3181e24124] [PMID] [PMCID] [DOI:10.1212/WNL.0b013e3181e24124]
11. Zhang Y, Zhang Y, Gu W, He L, Sun B. Th1/Th2 cell's function in immune system. Adv Exp Med Biol. 2014; 841:45-65. [DOI:10.1007/978-94-017-9487-9_3] [PMID] [DOI:10.1007/978-94-017-9487-9_3]
12. Fletcher JM, Lalor SJ, Sweeney CM, Tubridy N, Mills KH. T cells in Multiple Sclerosis and experimental autoimmune encephalomyelitis. Clin Exp Immunol. 2010; 162(1):1-11. [DOI:10.1111/j.1365-2249.2010.04143.x] [PMID] [PMCID] [DOI:10.1111/j.1365-2249.2010.04143.x]
13. Leray E, Moreau T, Fromont A, Edan G. Epidemiology of Multiple Sclerosis. Rev Neurol (Paris). 2016; 172(1):3-13. [DOI:10.1016/j.neurol.2015.10.006] [PMID] [DOI:10.1016/j.neurol.2015.10.006]
14. Etemadifar M, Sajjadi S, Nasr Z, Firoozeei TS, Abtahi SH, Akbari M, et al. Epidemiology of Multiple Sclerosis in Iran: a systematic review. Eur Neurol. 2013; 70(5-6):356-63. [DOI:10.1159/000355140] [PMID] [DOI:10.1159/000355140]
15. Burks JS, Bigley GK, Hill HH. Rehabilitation challenges in Multiple Sclerosis. Ann Indian Acad Neurol. 2009; 12(4):296-306. [DOI:10.4103/0972-2327.58273] [PMID] [PMCID] [DOI:10.4103/0972-2327.58273]
16. Lozano E, Dominguez-Villar M, Kuchroo V, Hafler DA. The TIGIT/CD226 axis regulates human T cell function. J Immunol. 2012; 188(8):3869-75. [DOI:10.4049/jimmunol.1103627] [PMID] [PMCID] [DOI:10.4049/jimmunol.1103627]
17. Maiti AK, Kim-Howard X, Viswanathan P, Guillen L, Qian X, Rojas-Villarraga A, et al. Non-synonymous variant (Gly307Ser) in CD226 is associated with susceptibility to multiple autoimmune diseases. Rheumatology (Oxford). 2010; 49(7):1239-44. [DOI:10.1093/rheumatology/kep470] [PMID] [PMCID] [DOI:10.1093/rheumatology/kep470]
18. Liu J, Qian X, Chen Z, Xu X, Gao F, Zhang S, et al. Crystal structure of cell adhesion molecule nectin-2/CD112 and its binding to immune receptor DNAM-1/CD226. J Immunol. 2012; 188(11):5511-20. [DOI:10.4049/jimmunol.1200324] [PMID] [DOI:10.4049/jimmunol.1200324]
19. Wagner AK, Kadri N, Snall J, Brodin P, Gilfillan S, Colonna M, et al. Expression of CD226 is associated to but not required for NK cell education. Nat Commun. 2017; 8:15627. [DOI:10.1038/ncomms15627] [PMID] [PMCID] [DOI:10.1038/ncomms15627]
20. Hou S, Ge K, Zheng X, Wei H, Sun R, Tian Z. CD226 protein is involved in immune synapse formation and triggers Natural Killer (NK) cell activation via its first extracellular domain. J Biol Chem. 2014; 289(10):6969-77. [DOI:10.1074/jbc.M113.498253] [PMID] [PMCID] [DOI:10.1074/jbc.M113.498253]
21. Gilfillan S, Chan CJ, Cella M, Haynes NM, Rapaport AS, Boles KS, et al. DNAM-1 promotes activation of cytotoxic lymphocytes by nonprofessional antigen-presenting cells and tumors. J Exp Med. 2008; 205(13):2965-73. [DOI:10.1084/jem.20081752] [PMID] [PMCID] [DOI:10.1084/jem.20081752]
22. Shibuya K, Shirakawa J, Kameyama T, Honda S, Tahara-Hanaoka S, Miyamoto A, et al. CD226 (DNAM-1) is involved in lymphocyte function-associated antigen 1 costimulatory signal for naive T cell differentiation and proliferation. J Exp Med. 2003; 198(12):1829-39. [DOI:10.1084/jem.20030958] [PMID] [PMCID] [DOI:10.1084/jem.20030958]
23. Lozano E, Joller N, Cao Y, Kuchroo VK, Hafler DA. The CD226/CD155 interaction regulates the proinflammatory (Th1/Th17)/anti-inflammatory (Th2) balance in humans. Journal of immunology. 2013; 191(7):3673-80. [DOI:10.4049/jimmunol.1300945] [PMID] [PMCID] [DOI:10.4049/jimmunol.1300945]
24. Avouac J, Elhai M, Tomcik M, Ruiz B, Friese M, Piedavent M, et al. Critical role of the adhesion receptor DNAX accessory molecule-1 (DNAM-1) in the development of inflammation-driven dermal fibrosis in a mouse model of systemic sclerosis. Ann Rheum Dis. 2013; 72(6):1089-98. [DOI:10.1136/annrheumdis-2012-201759] [PMID] [DOI:10.1136/annrheumdis-2012-201759]
25. Dardalhon V, Schubart AS, Reddy J, Meyers JH, Monney L, Sabatos CA, et al. CD226 is specifically expressed on the surface of Th1 cells and regulates their expansion and effector functions. J Immunol. 2005; 175(3):1558-65. [DOI:10.4049/jimmunol.175.3.1558] [PMID] [DOI:10.4049/jimmunol.175.3.1558]
26. Ye X, Zhang Z, Jiang Y, Han X, Wang Y, Zhang M, et al. Expression of human CD226 on T cells and natural killer cells and of soluble CD226 in plasma of HIV-1-infected Chinese patients. Viral Immunol. 2006; 19(3):576-81. [DOI:10.1089/vim.2006.19.576] [PMID] [DOI:10.1089/vim.2006.19.576]
27. Marum L, Miguel A, Ricardo CP, Miguel C. Reference gene selection for quantitative real-time PCR normalization in Quercus suber. PLoS One. 2012; 7(4):e35113. [DOI:10.1371/journal.pone.0035113] [PMID] [PMCID] [DOI:10.1371/journal.pone.0035113]
28. Kostić M. Role of Th1 and Th17 immune responces in pathogenesis of Multiple Sclerosis. Acta Med Medianae. 2010; 49(4):61-9.
29. Gross CC, Schulte-Mecklenbeck A, Rünzi A, Kuhlmann T, Posevitz-Fejfár A, Schwab N, et al. Impaired NK-mediated regulation of T-cell activity in Multiple Sclerosis is reconstituted by IL-2 receptor modulation. Proc Natl Acad Sci India Sect B Biol Sci. 2016; 113(21):E2973-E82. [DOI:10.1073/pnas.1524924113] [PMID] [PMCID] [DOI:10.1073/pnas.1524924113]
30. Dieudé P, Guedj M, Truchetet ME, Wipff J, Revillod L, Riemekasten G, et al. Association of the CD226 Ser307 variant with systemic sclerosis: Evidence of a contribution of costimulation pathways in systemic sclerosis pathogenesis. Arthritis Rheumatol. 2011; 63(4):1097-105. [DOI:10.1002/art.30204] [PMID] [DOI:10.1002/art.30204]
31. Wieczorek S, Hoffjan S, Chan A, Rey L, Harper L, Fricke H, et al. Novel association of the CD226 (DNAM-1) Gly307Ser polymorphism in Wegener's granulomatosis and confirmation for Multiple Sclerosis in German patients. Genes and immunity. 2009; 10(6):591-5. [DOI:10.1038/gene.2009.44] [PMID] [DOI:10.1038/gene.2009.44]
32. Löfgren SE, Delgado-Vega AM, Gallant CJ, Sánchez E, Frostegård J, Truedsson L, et al. A 3′-untranslated region variant is associated with impaired expression of CD226 in T and natural killer T cells and is associated with susceptibility to systemic lupus erythematosus. Arthritis Rheumatol. 2010; 62(11):3404-14. [DOI:10.1002/art.27677] [PMID] [DOI:10.1002/art.27677]
33. Qiu ZX, Zhang K, Qiu XS, Zhou M, Li WM. CD226 Gly307Ser association with multiple autoimmune diseases: A meta-analysis. Hum Immunol. 2013; 74(2):249-55. [DOI:10.1016/j.humimm.2012.10.009] [PMID] [DOI:10.1016/j.humimm.2012.10.009]
34. Ghavimi R, Alsahebfosoul F, Salehi R, Kazemi M, Etemadifar M, Zavaran Hosseini A. High-resolution melting curve analysis of polymorphisms within CD58, CD226, HLA-G genes and association with Multiple Sclerosis susceptibility in a subset of Iranian population: a case-control study. Acta Neurol Belg. 2018; 1-8. [DOI:10.1007/s13760-018-0992-y] [PMID] [DOI:10.1007/s13760-018-0992-y]
35. Yu X, Harden K, Gonzalez LC, Francesco M, Chiang E, Irving B, et al. The surface protein TIGIT suppresses T cell activation by promoting the generation of mature immunoregulatory dendritic cells. Nat Immunol. 2009; 10(1):48–57. [DOI:10.1038/ni.1674] [PMID] [DOI:10.1038/ni.1674]
36. Fuhrman CA, Yeh WI, Seay HR, Lakshmi PS, Chopra G, Zhang L, et al. Divergent phenotypes of human regulatory T cells expressing the receptors TIGIT and CD226. J Immunol. 2015; 195(1):145-55. [DOI:10.4049/jimmunol.1402381] [PMID] [PMCID] [DOI:10.4049/jimmunol.1402381]

Add your comments about this article : Your username or Email:
CAPTCHA code

Send email to the article author


© 2017 All Rights Reserved | Caspian Journal of Neurological Sciences

Designed & Developed by : Yektaweb