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Research Article

CTLA-4 Gene and the Susceptibility of Multiple Sclerosis: An Updated Meta-analysis Study Including 12,916 Cases and 15,455 Controls

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Pages 153-163 | Received 16 Jul 2013, Accepted 03 Jan 2014, Published online: 25 Mar 2014

REFERENCES

  • Andreevskiĭ, T. V., Sudomoina, M. A., Gusev, E. I., Boĭko, A. N., Alekseenkov, A. D., & Favorova, O. O. (2002). Polymorphism A/G in position + 49 of CTLA4 exon 1 in multiple sclerosis in Russians. Mol Biol (Mosk), 36, 643–648.
  • Bagos, P. G., Karnaouri, A. C., Nikolopoulos, G. K., & Hamodrakas, S. J. (2007). No evidence for association of CTLA-4 gene polymorphisms with the risk of developing multiple sclerosis: A meta-analysis. Mult Scler, 13, 156–168.
  • Bilińska, M., Frydecka, I., Noga, L., Dobosz, T., Zołedziewska, M., Suwalska, K., Tutak, A., & Pokryszko-Dragan, A. (2004). Progression of multiple sclerosis is associated with exon 1 CTLA-4 gene polymorphism. Acta Neurol Scand, 110, 67–71.
  • Borhani Haghighi, A., Ghahramani, S., Azarpira, N., Pourjafar, M., & Nikseresht, A. R. (2008). Cytotoxic T lymphocyte associated antigen-4 exon 1 A/G polymorphism in Iranian patients with multiple sclerosis. Eur J Neurol, 15, 862–864.
  • Brunet, J. F., Denizot, F., Luciani, M. F., Roux-Dosseto, M., Suzan, M., Mattei, M. G., & Golstein, P. (1987). A new member of the immunoglobulin superfamily-CTLA-4. Nature, 328, 267–270.
  • Chambers, C. A., Sullivan, T. J., & Allison, J. P. (1997). Lymphoproliferation in CTLA-4-deficient mice is mediated by costimulation-dependent activation of CD4 + T cells. Immunity, 7, 885–895.
  • Cizmarević, N. S., Gašparović, I., Peterlin, B., Sepčić, J., Rudolf, G., Kapović, M., Lavtar, P., & Ristić, S. (2011). CTLA-4 + 49 A/G gene polymorphism in Croatian and Slovenian multiple sclerosis patients. Int J Immunogenet, 38, 419–426.
  • Dincić, E., Zivković, M., Stanković, A., Obradović, D., Alavantić, D., Kostić, V., & Raicević, R. (2006). Association of polymorphisms in CTLA-4, IL-1ra and IL-1beta genes with multiple sclerosis in Serbian population. J Neuroimmunol, 177, 146–150.
  • Disanto, G., Morahan, J. M., Ramagopalan, S. V. (2012). Multiple sclerosis: Risk factors and their interactions. CNS Neurol Disord Drug Targets, 11, 545–555.
  • Ebers, G. (2013). Interactions of environment and genes in multiple sclerosis. J Neurol Sci,334, 161–163.
  • Fukazawa, T., Kikuchi, S., Miyagishi, R., Niino, M., Yabe, I., Hamada, T., & Sasaki, H. (2005). CTLA-4 gene polymorphism is not associated with conventional multiple sclerosis in Japanese. J Neuroimmunol, 159, 225–229.
  • Fukazawa, T., Yanagawa, T., Kikuchi, S., Yabe, I., Sasaki, H., Hamada, T., Miyasaka, K., Gomi, K., & Tashiro, K. (1999). CTLA-4 gene polymorphism may modulate disease in Japanese multiple sclerosis patients. J Neurol Sci, 171, 49–55.
  • Goodin, D. S. (2009)The causal cascade to multiple sclerosis: A model for MS pathogenesis. PLoS ONE, 4, e4565.
  • Greve, B., Simonenko, R., Illes, Z., Peterfalvi, A., Hamdi, N., Mycko, M. P., Selmaj K. W., Rozsa, C., Rajczy, K., Bauer, P., Berger, K., & Weissert, R. (2008). Multiple sclerosis and the CTLA4 autoimmunity polymorphism CT60: No association in patients from Germany, Hungary and Poland. Mult Scler, 14, 153–158.
  • Hader, W. J., Elliot, M., & Ebers, G. C. (1988). Epidemiology of multiple sclerosis in London and Middlesex County, Ontario, Canada. Neurology, 38, 617–621.
  • Hafler, D. (2004). Multiple sclerosis. J Clin Invest, 113, 788–794.
  • Harbo, H. F., Celius, E. G., Vartdal, F., & Spurkland, A. (1999). CTLA4 promoter and exon 1 dimorphisms in multiple sclerosis. Tissue Antigens, 53, 106–110.
  • Heggarty, S., Suppiah, V., Silversides, J., O’doherty, C., Droogan, A., McDonnell, G., Hawkins, S., Graham, C, & Vandenbroeck, K. (2007). CTLA4 gene polymorphisms and multiple sclerosis in Northern Ireland. J Neuroimmunol, 187, 187–191.
  • Heidari, A., Noori Daloii, M. R., Keramatipour, M., Rashikinezhad, A., Sahmani, A. A., & Amirzargar, A. A. (2010). CTLA-4 gene polymorphisms (− 318C/T, + 49A/G, + 6230A/G) in Iranian patients with multiple sclerosis. Iran J Allergy Asthma Immunol, 9, 219–223.
  • Kantarci, O. H., Hebrink, D. D., Achenbach, S. J., Atkinson, E. J., Waliszewska, A., Buckle, G., McMurray, C. T., de Andrade, M., Hafler, D. A., & Weinshenker, B. G. (2003). CTLA4 is associated with susceptibility to multiple sclerosis. J Neuroimmunol, 134, 133–141.
  • Khoury, S. J., Akalin, E., Chandraker, A., Turka, L. A., Linsley, P. S., Sayegh, M. H., & Hancock, W. W. (1995). CD28-B7 costimulatory blockade by CTLA4Ig prevents actively induced experimental autoimmune encephalomyelitis and inhibits Th1 but spares Th2 cytokines in the central nervous system. J Immunol, 155, 4521–4524.
  • Ligers, A., Xu, C., Saarinen, S., Hillert, J., & Olerup, O. (1999). The CTLA-4 gene is associated with multiple sclerosis. J Neuroimmunol, 97, 182–190.
  • Liu, J., & Zhang, H. (2013). − 1722T/C polymorphism (rs733618) of CTLA-4 significantly associated with systemic lupus erythematosus (SLE): A comprehensive meta-analysis. Hum Immunol, 74, 341–347.
  • Lorentzen, A. R., Celius, E. G., Ekstrøm, P. O., Wiencke, K, Lie, B. A., Myhr, K. M., Ling, V., Thorsby, E., Vartdal, F., Spurkland, A., & Harbo, H. F. (2005). Lack of association with the CD28/CTLA4/ICOS gene region among Norwegian multiple sclerosis patients. J Neuroimmunol, 166, 197–201.
  • Luomala, M., Lehtimäki, T., Huhtala, H., Ukkonen, M., Koivula, T., Hurme, M., & Elovaara, I. (2003). Promoter polymorphism of IL-10 and severity of multiple sclerosis. Acta Neurol Scand, 108, 396–400.
  • Malferrari, G., Stella, A., Monferini, E., Saltini, G., Proverbio, M. C, Grimaldi, L. M., Rossi-Bernardi, L, & Biunno, I. (2005). Ctla4 and multiple sclerosis in the Italian population. Exp Mol Pathol, 78, 55–57.
  • Mäurer, M., Ponath, A., Kruse, N., & Rieckmann, P. (2002). CTLA4 exon 1 dimorphism is associated with primary progressive multiple sclerosis. J Neuroimmunol, 131, 213–215.
  • Mkhikian, H., Grigorian, A., Li, C. F., Chen, H. L., Newton, B., Zhou, R. W., Beeton, C., Torossian, S., Tatarian, G. G., Lee, S. U., Lau, K., Walker, E., Siminovitch, K. A., Chandy, K. G., Yu, Z., Dennis, J. W., & Demetriou, M. (2011). Genetics and the environment converge to dysregulate N-glycosylation in multiple sclerosis. Nat Commun, 2, 334. doi: 10.1038/ncomms1333
  • Oksenberg, J. R., & Baranzini, S. E. (2010). Multiple sclerosis genetics—Is the glass half full, or half empty?Nat Rev Neurol, 6, 429–437.
  • Palacios, R., Comas, D., Elorza, J., & Villoslada, P. (2008). Genomic regulation of CTLA4 and multiple sclerosis. J Neuroimmunol, 203, 108–115.
  • Rasmussen, H. B., Kelly, M. A, Francis, D. A., & Clausen J. (2001). CTLA4 in multiple sclerosis. Lack of genetic association in a European Caucasian population but evidence of interaction with HLA-DR2 among Shanghai Chinese. J Neurol Sci,184, 143–147.
  • Stuart, R, Lovett-Racke, A. E., Frohman, E. M., Hawker, K., & Racke, M. K. (2007). Genetic analysis of the exon 1 position 49 CD152 dimorphism in multiple sclerosis. J Neuroimmunol, 191, 45–50.
  • Suppiah, V., Alloza, I., Heggarty, S., Goris, A., Dubois, B., Carton, H., & Vandenbroeck K. (2005). The CTLA4 + 49 A/G*G-CT60*G haplotype is associated with susceptibility to multiple sclerosis in Flanders. J Neuroimmunol, 164, 148–153.
  • Teutsch, S. M., Booth, D. R., Bennetts, B. H., Heard, R. N., & Stewart, G. J. (2004). Association of common T cell activation gene polymorphisms with multiple sclerosis in Australian patients. J Neuroimmunol, 148, 218–230.
  • van Veen, T., Crusius, J. B., van Winsen, L., Xia, B., Barkhof, F., Salvador Peña, A, Polman, C. H., & Uitdehaag, B. M. (2003). CTLA-4 and CD28 gene polymorphisms in susceptibility, clinical course and progression of multiple sclerosis. J Neuroimmunol, 140, 188–193.
  • Wray, B. N., Stankovich, J., Whittock, L., Dwyer, T., Ponsonby, A. L., van der Mei, I. A., Taylor, B., Dickinson, J., Foote, S., & McMorran, B. J. (2008). CTLA-4 and multiple sclerosis: The A49G single nucleotide polymorphism shows no association with multiple sclerosis in a Southern Australian population. J Neuroimmunol, 196, 139–142.
  • Xuan, C., Zhang, B. B., Li, M., Deng, K. F., Yang, T, & Zhang, X. E. (2011). No association between APOE epsilon 4 allele and multiple sclerosis susceptibility: A meta-analysis from 5472 cases and 4727 controls. J Neurol Sci, 308, 110–116.
  • Yousefipour, G., Erfani, N., Momtahan, M., Moghaddasi, H., & Ghaderi, A. (2009). CTLA4 exon 1 and promoter polymorphisms in patients with multiple sclerosis. Acta Neurol Scand, 120, 424–429.
  • Zamvil, S., Nelson, P., Trotter, J., Mitchell, D., Knobler, R., Fritz, R., & Steinman, L. (1985). T-cell clones specific for myelin basic protein induce chronic relapsing paralysis and demyelination. Nature, 317, 355–358.

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