CTLA-4 CT60 (rs3087243) polymorphism and autoimmune thyroid diseases susceptibility: a comprehensive meta-analysis

References

• Wang C, Crapo LM. The epidemiology of thyroid disease and implications for screening. Endocrinol Metab Clin North Am 1997;26:189–218
   PubMed Web of Science ®Google Scholar
• Jacobson DL, Gange SJ, Rose NR, et al. Epidemiology and estimated population burden of selected autoimmune diseases in the United States. Clin Immuno Immunopathol 1997;84:223–43
   PubMedGoogle Scholar
• Sahin M, Gursoy A, Erdogan MF. Cytotoxic T lymphocyte-associated molecule-4 polymorphism in Turkish patients with Hashimoto thyroiditis. Int J Immunogenet 2009;36:103–6
   PubMedGoogle Scholar
• Weetman AP. Autoimmune thyroid disease propagation and progression. Eur J Endocrinol 2003;148:1–9
   PubMed Web of Science ®Google Scholar
• Lee HS, Kang J, Yang S, et al. Susceptibility influence of a PTPN22 haplotype with thyroid autoimmunity in Koreans. Diabetes Metab Res Rev 2011;27:878–82
   Google Scholar
• Pastuszak-Lewandoska D, Sewerynek E, Domanska D, et al. CTLA-4 gene polymorphisms and their influence on predisposition to autoimmune thyroid diseases (Graves’ disease and Hashimoto’s thyroiditis). Arch Med Sci 2012;8:415–21
   Google Scholar
• Maierhaba M, Zhang JA, Yu ZY, et al. Association of the thyroglobulin gene polymorphism with autoimmune thyroid disease in Chinese population. Endocrine 2008;33:294–9
   PubMed Web of Science ®Google Scholar
• Vaidya B, Taylor P, Pearce S. The genetics of autoimmune thyroid disease. J Clin Endocrinol Metab 2002;87:5385–97
   PubMed Web of Science ®Google Scholar
• Ueda H, Howson JM, Esposito L, et al. Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease. Nature 2003;423:506–11
   PubMed Web of Science ®Google Scholar
• Heward JM, Allahabadia A, Carr-Smith J, et al. No evidence for allelic association of a human CTLA-4 promoter polymorphism with autoimmune thyroid disease in either population-based case-control or family-based studies. Clin Endocrinol (Oxf) 1998;49:331–4
   PubMedGoogle Scholar
• Greenfield EA, Nguyen KA, Kuchroo VK. CD28/B7 costimulation: a review. Crit Rev Immunol 1998;18:389–418
   PubMed Web of Science ®Google Scholar
• Si X, Zhang X, Tang W, et al. Association between the CTLA-4 +49A/G polymorphism and Graves’ disease: a meta-analysis. Exp Ther Med 2012;4:538–44
   Google Scholar
• Chong KK, Chiang SW, Wong GW, et al. Association of CTLA-4 and IL-13 gene polymorphisms with Graves’ disease and ophthalmopathy in Chinese children. Invest Ophthalmol Vis Sci 2008;49:2409–15
   PubMed Web of Science ®Google Scholar
• Zaletel K, Krhin B, Gaberscek S, et al. Association of CT60 cytotoxic T lymphocyte antigen-4 gene polymorphism with thyroid autoantibody production in patients with Hashimoto’s and postpartum thyroiditis. Clin Exp Immunol 2010;161:41–7
   PubMedGoogle Scholar
• Kavvoura FK, Akamizu T, Awata T, et al. Cytotoxic T-Lymphocyte associated antigen 4 gene polymorphisms and autoimmune thyroid disease: a meta-analysis. J Clin Endocrinol Metab 2007;92:3162–70
   PubMed Web of Science ®Google Scholar
• Mantel N, Haenszel W. Statistical aspects of the analysis of data from retrospective studies of disease. J Natl Cancer Inst 1959;22:19–48
   PubMedGoogle Scholar
• DerSimonian R, Laird N. Meta-analysis in clinical trials. Control Clin Trials 1986;7:177–88
   PubMed Web of Science ®Google Scholar
• Duval S, Tweedie R. Trim and fill: a simple funnel plot-based method of testing and adjusting for publication bias in meta-analysis. Biometrics 2000;56:455–63
   PubMed Web of Science ®Google Scholar
• Weng YC, Wu MJ, Lin WS. CT 60 single nucleotide polymorphism of the CTLA-4 gene is associated with susceptibility to Graves’ disease in the Taiwanese population. Ann Clin Lab Sci 2005;35:259–64
   Google Scholar
• Petrone A, Giorgi G, Galgan A, et al. CT60 single nucleotide polymorphisms of the cytotoxic T-lymphocyte-associated antigen-4 gene region is associated with graves’ disease in an Italian population. Thyroid 2005;15:232–8
   PubMed Web of Science ®Google Scholar
• Ban Y, Tozaki T, Taniyama M, et al. Association of a CTLA-4 3′ untranslated region (CT60) single nucleotide polymorphism with autoimmune thyroid disease in the Japanese population. Autoimmunity 2005;38:151–3
   PubMed Web of Science ®Google Scholar
• Cho HJ, Chung JH, Kim IS, et al. Lack of a genetic association between the CTLA-4 gene and Graves’ disease in Koreans. Thyroid 2006;16:237–41
   Google Scholar
• Wang PW, Chen IY, Liu RT, et al. Cytotoxic T lymphocyte-associated molecule-4 gene polymorphism and hyperthyroid Graves’ disease relapse after antithyroid drug withdrawal: a follow-up study. J Clin Endocrinol Metab 2007;92:2513–18
   Google Scholar
• Tsai ST, Huang CY, Lo FS, et al. Association of CT60 polymorphism of the CTLA4 gene with Graves’ disease in Taiwanese children. J Pediatr Endocrinol Metab 2008;21:665–72
   Google Scholar
• Kimura H, Kato Y, Shimizu S, et al. Association of polymorphism at position 49 in exon 1 of the cytotoxic T-lymphocyte-associated factor 4 gene with Graves’ disease refractory to medical treatment, but not with amiodarone-associated thyroid dysfunction. Thyroid 2009;19:975–81
   Google Scholar
• Bicek A, Zaletel K, Gaberscek S, et al. 49A/G and CT60 polymorphisms of the cytotoxic T-lymphocyte-associated antigen 4 gene associated with autoimmune thyroid disease. Hum Immunol 2009;70:820–4
   PubMed Web of Science ®Google Scholar
• Kimkong I, Nakkuntod J, Sae-Ngow S, et al. Association between CTLA-4 polymorphisms and the susceptibility to systemic lupus erythematosus and Graves’ disease in Thai population. Asian Pac J Allergy Immunol 2011;29:229–35
   PubMed Web of Science ®Google Scholar
• Han S, Zhang S, Zhang W, et al. CTLA4 polymorphisms and ophthalmopathy in Graves’ disease patients: association study and meta-analysis. Hum Immunol 2006;67:618–26
   PubMed Web of Science ®Google Scholar
• Ikegami H, Awata T, Kawasaki E, et al. The association of CTLA4 polymorphism with type 1 diabetes is concentrated in patients complicated with autoimmune thyroid disease: a multicenter collaborative study in Japan. J Chin Endocrinol Metab 2006;91:1087–92
   PubMedGoogle Scholar
• Dollos T, Avbelj M, Barak L, et al. CTLA-4 gene polymorphism predispose to autoimmune endocrinopathies but not to celiac disease. Neuro Endocrinol Lerr 2008;29:334–40
   Google Scholar
• Chistiakov DA. Immunogenetics of Hashimoto’s thyroiditis. J Autoimmune Dis 2005;2:1–21
   PubMedGoogle Scholar
• Brix TH, Kyvik KO, Christensen K, et al. Evidence for a major role of heredity in Grave’s disease: a population-bases study of two Danish twin cohorts. J Clin Endocrinol Metab 2001;86:930–4
   PubMed Web of Science ®Google Scholar
• Vos XG, Endert E, Tijssen JG, et al. Genotypes in relation to phenotypic appearance and exposure to environmental factors in Graves’ hyperthyroidism. Eur J Endocrinol 2012;167:783–92
   Google Scholar
• Takahashi M, Kimura A. HLA and CTLA4 polymorphism may confer a synergistic risk in the susceptibility to Graves’ disease. J Hum Genet 2010;55:323–6
   Google Scholar
• Phenekos C, Vryonidou A, Gritzapis AD, et al. Th1 and Th2 serum cytokine profiles characterize patients with Hashimoto’s thyroiditis (Th1) and Graves’ disease (Th2). Neuroimmunomodulation 2004;11:209–13
   PubMed Web of Science ®Google Scholar
• Waterhouse P, Penninger JM, Timms E, et al. Lymphoproliferative disorders with early lethality in mice deficient in CTLA-4. Science 1995;270:985–8
   PubMed Web of Science ®Google Scholar
• Ye F, Hou P, Wu X, et al. The significance of immune-related molecule expression profiles in an animal model of Graves’ disease. Autoimmunity 2012;45:143–52
   PubMed Web of Science ®Google Scholar
• Mao C, Wang S, Xiao Y, et al. Impairment of regulatory capacity of CD4 + CD25+ regulatory T cells mediated by dendritic cell polarization and hyperthyroidism in Graves’ disease. J Immunol 2011;186:4734–43
   PubMed Web of Science ®Google Scholar
• Takahashi T, Tagami T, Yamazaki S, et al. Immunologic self-tolerance maintained by CD25 (+) CD4 (+) regulatory T cells constitutively expressing cytotoxic-T-lymphocyte-associated antigen 4. J Exp Med 2000;192:303–10
   PubMed Web of Science ®Google Scholar
• Daroszewski J, Pawlak E, Karabon L, et al. Soluble CTLA-4 receptor an immunological marker of Graves’ disease and severity of ophthalmopathy is associated with CTLA-4 Jo31 and CT60 gene polymorphisms. Eur J Endocrinol 2009;161:787–93
   PubMed Web of Science ®Google Scholar
• Du L, Yang J, Huang J, et al. The associations between the polymorphisms in the CTLA-4 gene and the risk of Graves’ disease in the Chinese population. BMC Med Genet 2013;14:46
   Google Scholar
• Inoue N, Watanabe M, Yamada H, et al. Associations between autoimmune thyroid disease prognosis and functional polymorphisms of susceptibility genes, CTLA4, PTPN22, CD40, FCRL3, and ZFAT, previously revealed in genome-wide association studies. J Clin Immunol 2012;32:1243–52
   PubMed Web of Science ®Google Scholar
• Song GG, Kim JH, Lee YH. The CTLA-4 +49 A/G, CT60 A/G and PTPN 22 1858 C/T polymorphisms and susceptibility to vitiligo: a meta-analysis. Mol Biol Rep 2013;40:2985–93
   Google Scholar
• Zhu JM, Li BK, Chen GM, et al. CTLA-4-1722 T/C polymorphism and systemic lupus erythematosus susceptibility: a meta-analysis involving ten separate studies. Immunol Invest 2013;42:91–105
   PubMed Web of Science ®Google Scholar