Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2017, Article ID 3916395, 8 pages
https://doi.org/10.1155/2017/3916395
Review Article

General and Specific Genetic Polymorphism of Cytokines-Related Gene in AITD

1Department of General Surgery, Dongzhimen Hospital of Beijing University of Chinese Medicine, Beijing, China
2State Key Laboratory of Toxicology and Medical Countermeasures, Beijing Institute of Pharmacology and Toxicology, Beijing, China
3Department of Medical Service, The Third Clinical Medical College, Beijing University of Chinese Medicine, Beijing, China

Correspondence should be addressed to Ding Zhiguo; moc.361@1_ougihzgnid

Received 14 October 2016; Revised 4 December 2016; Accepted 12 December 2016; Published 4 January 2017

Academic Editor: Jun-hui Wang

Copyright © 2017 Chen Xiaoheng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. O. Eber and W. Langsteger, “Clinical aspects of autoimmune thyroid diseases,” Acta Medica Austriaca, vol. 21, no. 1, pp. 1–7, 1994. View at Google Scholar · View at Scopus
  2. H. Li and T. Wang, “The autoimmunity in Graves's disease,” Frontiers in Bioscience, vol. 18, no. 2, pp. 782–787, 2013. View at Publisher · View at Google Scholar · View at Scopus
  3. F. Orsini, A. C. Traino, M. Grosso et al., “Personalization of radioiodine treatment for Graves' disease: a prospective, randomized study with a novel method for calculating the optimal131I-iodide activity based on target reduction of thyroid mass,” Quarterly Journal of Nuclear Medicine and Molecular Imaging, vol. 56, no. 6, pp. 496–502, 2012. View at Google Scholar · View at Scopus
  4. M. Rotondi, L. Chiovato, S. Romagnani, M. Serio, and P. Romagnani, “Role of chemokines in endocrine autoimmune diseases,” Endocrine Reviews, vol. 28, no. 5, pp. 492–520, 2007. View at Publisher · View at Google Scholar · View at Scopus
  5. A. J. Klecha, M. L. Barreiro Arcos, L. Frick, A. M. Genaro, and G. Cremaschi, “Immune-endocrine interactions in autoimmune thyroid diseases,” NeuroImmunoModulation, vol. 15, no. 1, pp. 68–75, 2008. View at Publisher · View at Google Scholar · View at Scopus
  6. S. M. McLachlan and B. Rapoport, “Breaking tolerance to thyroid antigens: changing concepts in thyroid autoimmunity,” Endocrine Reviews, vol. 35, no. 1, pp. 59–105, 2014. View at Publisher · View at Google Scholar · View at Scopus
  7. D. Wamala, H. K. Buteme, S. Kirimunda, G. Kallenius, and M. Joloba, “Association between human leukocyte antigen class II and pulmonary tuberculosis due to mycobacterium tuberculosis in Uganda,” BMC Infectious Diseases, vol. 16, article 23, 2016. View at Publisher · View at Google Scholar · View at Scopus
  8. N. Erdmann, V. Y. Du, J. Carlson et al., “HLA class-II associated HIV polymorphisms predict escape from CD4+ T cell responses,” PLoS Pathogens, vol. 11, no. 8, Article ID e1005111, 2015. View at Publisher · View at Google Scholar · View at Scopus
  9. S. Shrestha, H. W. Wiener, B. Aissani, A. Shendre, J. Tang, and M. A. Portman, “Imputation of class I and II HLA loci using high-density SNPs from ImmunoChip and their associations with Kawasaki disease in family-based study,” International Journal of Immunogenetics, vol. 42, no. 3, pp. 140–146, 2015. View at Publisher · View at Google Scholar · View at Scopus
  10. L. A. M. Smit, D. P. Strachan, R. Vermeulen et al., “Human leukocyte antigen class II variants and adult-onset asthma: does occupational allergen exposure play a role?” The European Respiratory Journal, vol. 44, no. 5, pp. 1234–1242, 2014. View at Publisher · View at Google Scholar · View at Scopus
  11. S. M. McLachlan, “The genetic basis of autoimmune thyroid disease: time to focus on chromosomal loci other than the major histocompatibility complex (HLA in man),” The Journal of Clinical Endocrinology & Metabolism, vol. 77, no. 3, pp. 605A–605C, 1993. View at Publisher · View at Google Scholar
  12. C. B. Sanjeevi, C. DeWeese, M. Landin-Olsson et al., “Analysis of critical residues of HLA-DQ6 molecules in insulin-dependent diabetes mellitus,” Tissue Antigens, vol. 50, no. 1, pp. 61–65, 1997. View at Publisher · View at Google Scholar · View at Scopus
  13. A. B. T. Barlow, N. Wheatcroft, P. Watson, and A. P. Weetman, “Association of HLA-DQA10501 with Graves' disease in English Caucasian men and women,” Clinical Endocrinology, vol. 44, no. 1, pp. 73–77, 1996. View at Publisher · View at Google Scholar · View at Scopus
  14. T. Yanagawa, Y. Hidaka, V. Guimaraes, M. Soliman, and L. J. DeGroot, “CTLA-4 gene polymorphism associated with Graves' disease in a Caucasian population,” Journal of Clinical Endocrinology and Metabolism, vol. 80, no. 1, pp. 41–45, 1995. View at Google Scholar · View at Scopus
  15. F. K. Kavvoura, T. Akamizu, T. Awata et al., “Cytotoxic T-lymphocyte associated antigen 4 gene polymorphisms and autoimmune thyroid disease: a meta-analysis,” Journal of Clinical Endocrinology and Metabolism, vol. 92, no. 8, pp. 3162–3170, 2007. View at Publisher · View at Google Scholar · View at Scopus
  16. P.-W. Wang, I.-Y. Chen, R.-T. Liu, C.-J. Hsieh, E. Hsi, and S.-H. H. Juo, “Cytotoxic T lymphocyte-associated molecule-4 gene polymorphism and hyperthyroid Graves' disease relapse after antithyroid drug withdrawal: a follow-up study,” The Journal of Clinical Endocrinology & Metabolism, vol. 92, no. 7, pp. 2513–2518, 2007. View at Publisher · View at Google Scholar · View at Scopus
  17. M. Sahin, M. F. Erdogan, and G. Erdogan, “Cytotoxic T lymphocyte-associated molecule-4 polymorphisms in Turkish Graves' disease patients and association with probability of remission after antithyroid therapy,” European Journal of Internal Medicine, vol. 16, no. 5, pp. 352–355, 2005. View at Publisher · View at Google Scholar · View at Scopus
  18. Y. Kinjo, N. Takasu, I. Komiya et al., “Remission of Graves' hyperthyroidism and A/G polymorphism at position 49 in exon 1 of cytotoxic T lymphocyte-associated molecule-4 gene,” Journal of Clinical Endocrinology and Metabolism, vol. 87, no. 6, pp. 2593–2596, 2002. View at Publisher · View at Google Scholar · View at Scopus
  19. J.-F. Brunet, F. Denizot, M.-F. Luciani et al., “A new member of the immunoglobulin superfamily—CTLA-4,” Nature, vol. 328, no. 6127, pp. 267–270, 1987. View at Publisher · View at Google Scholar · View at Scopus
  20. A. Kosmaczewska, L. Ciszak, D. Boćko, and I. Frydecka, “Expression and functional significance of CTLA-4, a negative regulator of T cell activation,” Archivum Immunologiae et Therapiae Experimentalis, vol. 49, no. 1, pp. 39–46, 2001. View at Google Scholar · View at Scopus
  21. K.-M. Lee, E. Chuang, M. Griffin et al., “Molecular basis of T cell inactivation by CTLA-4,” Science, vol. 282, no. 5397, pp. 2263–2266, 1998. View at Publisher · View at Google Scholar · View at Scopus
  22. B. K. Finck, P. S. Linsley, and D. Wofsy, “Treatment of murine lupus with CTLA4Ig,” Science, vol. 265, no. 5176, pp. 1225–1227, 1994. View at Publisher · View at Google Scholar · View at Scopus
  23. P. S. Linsley, J. L. Greene, W. Brady et al., “Human B7-1 (CD80) and B7-2 (CD86) bind with similar avidities but distinct kinetics to CD28 and CTLA-4 receptors,” Immunity, vol. 1, no. 9, pp. 793–801, 1994. View at Publisher · View at Google Scholar
  24. D. J. Lenschow, K. C. Herold, L. Rhee et al., “CD28/B7 regulation of Th1 and Th2 subsets in the development of autoimmune diabetes,” Immunity, vol. 5, no. 3, pp. 285–293, 1996. View at Publisher · View at Google Scholar
  25. T. Kouki, Y. Sawai, C. A. Gardine, M.-E. Fisfalen, M.-L. Alegre, and L. J. DeGroot, “CTLA-4 Gene polymorphism at position 49 in exon 1 reduces the inhibitory function of CTLA-4 and contributes to the pathogenesis of Graves' disease,” Journal of Immunology, vol. 165, no. 11, pp. 6606–6611, 2000. View at Publisher · View at Google Scholar · View at Scopus
  26. Y. Ban, T. F. Davies, D. A. Greenberg et al., “Analysis of the CTLA-4, CD28, and inducible costimulator (ICOS) genes in autoimmune thyroid disease,” Genes and Immunity, vol. 4, no. 8, pp. 586–593, 2003. View at Publisher · View at Google Scholar · View at Scopus
  27. M. Mäurer, S. Loserth, A. Kolb-Mäurer et al., “A polymorphism in the human cytotoxic T-lymphocyte antigen 4 (CTLA4) gene (exon 1 +49) alters T-cell activation,” Immunogenetics, vol. 54, no. 1, pp. 1–8, 2002. View at Publisher · View at Google Scholar · View at Scopus
  28. M. Takara, T. Kouki, and L. J. DeGroot, “CTLA-4 AT-repeat polymorphism reduces the inhibitory function of CTLA-4 in Graves' disease,” Thyroid, vol. 13, no. 12, pp. 1083–1089, 2003. View at Publisher · View at Google Scholar · View at Scopus
  29. S. Anjos, A. Nguyen, H. Ounissi-Benkalha, M.-C. Tessier, and C. Polychronakos, “A common autoimmunity predisposing signal peptide variant of the cytotoxic T-lymphocyte antigen 4 results in inefficient glycosylation of the susceptibility allele,” Journal of Biological Chemistry, vol. 277, no. 48, pp. 46478–46486, 2002. View at Publisher · View at Google Scholar · View at Scopus
  30. A. Bossowski, A. Stasiak-Barmuta, M. Urban, and C. Rinderle, “Analysis of costimulatory molecules (CD28-CTLA-4/B7) expression on chosen mononuclear cells in adolescents with Graves' disease during methimazole therapy,” Endokrynologia, Diabetologia i Choroby Przemiany Materii Wieku Rozwojowego, vol. 10, no. 2, pp. 93–101, 2004. View at Google Scholar · View at Scopus
  31. A. Bossowski, A. Stasiak-Barmuta, and M. Urban, “Relationship between CTLA-4 and CD28 molecule expression on T lymphocytes and stimulating and blocking autoantibodies to the TSH-receptor in children with Graves' disease,” Hormone Research, vol. 64, no. 4, pp. 189–197, 2005. View at Publisher · View at Google Scholar · View at Scopus
  32. R. J. Hill, S. Zozulya, Y.-L. Lu, K. Ward, M. Gishizky, and B. Jallal, “The lymphoid protein tyrosine phosphatase Lyp interacts with the adaptor molecule Grb2 and functions as a negative regulator of T-cell activation,” Experimental Hematology, vol. 30, no. 3, pp. 237–244, 2002. View at Publisher · View at Google Scholar · View at Scopus
  33. V. Pradhan, V. Borse, and K. Ghosh, “PTPN22 gene polymorphisms in autoimmune diseases with special reference to systemic lupus erythematosus disease susceptibility,” Journal of Postgraduate Medicine, vol. 56, no. 3, pp. 239–242, 2010. View at Publisher · View at Google Scholar · View at Scopus
  34. M. Rieck, A. Arechiga, S. Onengut-Gumuscu, C. Greenbaum, P. Concannon, and J. H. Buckner, “Genetic variation in PTPN22 corresponds to altered function of T and B lymphocytes,” The Journal of Immunology, vol. 179, no. 7, pp. 4704–4710, 2007. View at Publisher · View at Google Scholar · View at Scopus
  35. J. Zikherman, M. Hermiston, D. Steiner, K. Hasegawa, A. Chan, and A. Weiss, “PTPN22 deficiency cooperates with the CD45 E613R allele to break tolerance on a non-autoimmune background,” The Journal of Immunology, vol. 182, no. 7, pp. 4093–4106, 2009. View at Publisher · View at Google Scholar · View at Scopus
  36. R. J. Brownlie, L. A. Miosge, D. Vassilakos, L. M. Svensson, A. Cope, and R. Zamoyska, “Lack of the phosphatase PTPN22 increases adhesion of murine regulatory T cells to improve their immunosuppressive function,” Science Signaling, vol. 5, no. 252, article ra87, 2012. View at Publisher · View at Google Scholar · View at Scopus
  37. M. B. Ladner, N. Bottini, A. M. Valdes, and J. A. Noble, “Association of the single nucleotide polymorphism C1858T of the PTPN22 gene with type 1 diabetes,” Human Immunology, vol. 66, no. 1, pp. 60–64, 2005. View at Publisher · View at Google Scholar · View at Scopus
  38. M. R. Velaga, V. Wilson, C. E. Jennings et al., “The codon 620 tryptophan allele of the lymphoid tyrosine phosphatase (LYP) gene is a major determinant of Graves' disease,” The Journal of Clinical Endocrinology & Metabolism, vol. 89, no. 11, pp. 5862–5865, 2004. View at Publisher · View at Google Scholar · View at Scopus
  39. Y. H. Lee, Y. H. Rho, S. J. Choi et al., “The PTPN22 C1858T functional polymorphism and autoimmune diseases—a meta-analysis,” Rheumatology, vol. 46, no. 1, pp. 49–56, 2007. View at Publisher · View at Google Scholar · View at Scopus
  40. Y. Kochi, R. Yamada, A. Suzuki et al., “A functional variant in FCRL3, encoding Fc receptor-like 3, is associated with rheumatoid arthritis and several autoimmunities,” Nature Genetics, vol. 37, pp. 478–485, 2005. View at Publisher · View at Google Scholar
  41. M.-J. Xu, R. Zhao, H. Cao, and Z. J. Zhao, “SPAP2, an Ig family receptor containing both ITIMs and ITAMs,” Biochemical and Biophysical Research Communications, vol. 293, no. 3, pp. 1037–1046, 2002. View at Publisher · View at Google Scholar · View at Scopus
  42. R. S. Davis, Y.-H. Wang, H. Kubagawa, and M. D. Cooper, “Identification of a family of Fc receptor homologs with preferential B cell expression,” Proceedings of the National Academy of Sciences of the United States of America, vol. 98, no. 17, pp. 9772–9777, 2001. View at Publisher · View at Google Scholar · View at Scopus
  43. A. Martinez, E. Sanchez, A. Valdivia et al., “Epistatic interaction between FCRL3 and NF B1 genes in Spanish patients with rheumatoid arthritis,” Annals of the Rheumatic Diseases, vol. 65, no. 9, pp. 1188–1191, 2006. View at Publisher · View at Google Scholar
  44. M. Itoh, K. Uchimura, M. Makino et al., “Production of IL-10 and IL-12 in CD40 and interleukin 4-activated mononuclear cells from patients with Graves' disease,” Cytokine, vol. 12, no. 6, pp. 688–693, 2000. View at Publisher · View at Google Scholar · View at Scopus
  45. Y. Hidaka, M. Okumura, S. Fukata et al., “Increased serum concentration of interleukin-12 in patients with silent thyroiditis and Graves' disease,” Thyroid, vol. 9, no. 2, pp. 149–153, 1999. View at Publisher · View at Google Scholar · View at Scopus
  46. T. Hoshino, H. Yagita, J. R. Ortaldo, R. H. Wiltrout, and H. A. Young, “In vivo administration of IL-18 can induce IgE production through Th2 cytokine induction and up-regulation of CD40 ligand (CD154) expression on CD4+ T cells,” European Journal of Immunology, vol. 30, no. 7, pp. 1998–2006, 2000. View at Publisher · View at Google Scholar · View at Scopus
  47. T. M. Foy, A. Aruffo, J. Bajorath, J. E. Buhlmann, and R. J. Noelle, “Immune regulation by CD40 and its ligand GP39,” Annual Review of Immunology, vol. 14, pp. 591–617, 1996. View at Publisher · View at Google Scholar · View at Scopus
  48. A. Kumanogoh, X. Wang, I. Lee et al., “Increased T cell autoreactivity in the absence of CD40-CD40 ligand interactions: a role of CD40 in regulatory T cell development,” The Journal of Immunology, vol. 166, no. 1, pp. 353–360, 2001. View at Publisher · View at Google Scholar · View at Scopus
  49. R. A. Metcalfe, R. S. McIntosh, F. Marelli-Berg, G. Lombardi, R. Lechler, and A. P. Weetman, “Detection of CD40 on human thyroid follicular cells: analysis of expression and function,” Journal of Clinical Endocrinology and Metabolism, vol. 83, no. 4, pp. 1268–1274, 1998. View at Publisher · View at Google Scholar · View at Scopus
  50. J. Mysliwiec, M. Oklota, A. Nikolajuk, D. Waligorski, and M. Gorska, “Serum CD40/CD40L system in Graves' disease and Hashimoto's thyroiditis related to soluble Fas, FasL and humoral markers of autoimmune response,” Immunological Investigations, vol. 36, no. 3, pp. 247–257, 2007. View at Publisher · View at Google Scholar · View at Scopus
  51. B. Quadbeck, A. K. Eckstein, S. Tews et al., “Maturation of thyroidal dendritic cells in Graves' disease,” Scandinavian Journal of Immunology, vol. 55, no. 6, pp. 612–620, 2002. View at Publisher · View at Google Scholar · View at Scopus
  52. Y. Nakamoto, M. Niki, M. Watanabe, and Y. Iwatani, “Increase in immunoglobulin G3-secreting cells in intractable Graves' disease,” Thyroid, vol. 13, no. 4, pp. 325–331, 2003. View at Publisher · View at Google Scholar · View at Scopus
  53. G. Carayanniotis, S. R. Masters, and R. J. Noelle, “Suppression of murine thyroiditis via blockade of the CD40-CD40L interaction,” Immunology, vol. 90, no. 3, pp. 421–426, 1997. View at Publisher · View at Google Scholar · View at Scopus
  54. A. Shibaki and S. I. Katz, “Activation through CD40 ligation induces functional Fas ligand expression by Langerhans cells,” European Journal of Immunology, vol. 31, no. 10, pp. 3006–3015, 2001. View at Publisher · View at Google Scholar · View at Scopus
  55. H. Ueda, J. M. M. Howson, L. Esposito et al., “Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease,” Nature, vol. 423, no. 6939, pp. 506–511, 2003. View at Publisher · View at Google Scholar · View at Scopus
  56. Y. J. Park, H. K. Chung, D. J. Park et al., “Polymorphism in the promoter and exon 1 of the cytotoxic T lymphocyte antigen-4 gene associated with autoimmune thyroid disease in Koreans,” Thyroid, vol. 10, no. 6, pp. 453–459, 2000. View at Google Scholar · View at Scopus
  57. B. Vaidya and S. Pearce, “The emerging role of the CTLA-4 gene in autoimmune endocrinopathies,” European Journal of Endocrinology, vol. 150, no. 5, pp. 619–626, 2004. View at Publisher · View at Google Scholar · View at Scopus
  58. Y. Ban, D. A. Greenberg, E. Concepcion, L. Skrabanek, R. Villanueva, and Y. Tomer, “Amino acid substitutions in the thyroglobulin gene are associated with susceptibility to human and murine autoimmune thyroid disease,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 25, pp. 15119–15124, 2003. View at Publisher · View at Google Scholar · View at Scopus
  59. Y. Ban, T. Tozaki, M. Taniyama, M. Tomita, and Y. Ban, “Association of a CTLA-4 3′ untranslated region (CT60) single nucleotide polymorphism with autoimmune thyroid disease in the Japanese population,” Autoimmunity, vol. 38, no. 2, pp. 151–153, 2005. View at Publisher · View at Google Scholar · View at Scopus
  60. K. Zaletel, B. Krhin, S. Gaberšček, E. Pirnat, and S. Hojker, “The influence of the exon 1 polymorphism of the cytotoxic T lymphocyte antigen 4 gene on thyroid antibody production in patients with newly diagnosed Graves' disease,” Thyroid, vol. 12, no. 5, pp. 373–376, 2002. View at Publisher · View at Google Scholar · View at Scopus
  61. K. Zaletel, B. Krhin, S. Gaberšček, A. Biček, T. Pajič, and S. Hojker, “Association of CT60 cytotoxic T lymphocyte antigen-4 gene polymorphism with thyroid autoantibody production in patients with Hashimoto's and postpartum thyroiditis,” Clinical & Experimental Immunology, vol. 161, no. 1, pp. 41–47, 2010. View at Publisher · View at Google Scholar · View at Scopus
  62. S. Onengut-Gumuscu, K. G. Ewens, R. S. Spielman, and P. Concannon, “A functional polymorphism (1858C/T) in the PTPN22 gene is linked and associated with type I diabetes in multiplex families,” Genes and Immunity, vol. 5, no. 8, pp. 678–680, 2004. View at Publisher · View at Google Scholar · View at Scopus
  63. A. B. Begovich, V. E. H. Carlton, L. A. Honigberg et al., “A missense single-nucleotide polymorphism in a gene encoding a protein tyrosine phosphatase (PTPN22) is associated with rheumatoid arthritis,” American Journal of Human Genetics, vol. 75, no. 2, pp. 330–337, 2004. View at Publisher · View at Google Scholar · View at Scopus
  64. M. K. Viken, S. S. Amundsen, T. K. Kvien et al., “Association analysis of the 1858C > T polymorphism in the PTPN22 gene in juvenile idiopathic arthritis and other autoimmune diseases,” Genes and Immunity, vol. 6, no. 3, pp. 271–273, 2005. View at Publisher · View at Google Scholar · View at Scopus
  65. C. Kyogoku, C. D. Langefeld, W. A. Ortmann et al., “Genetic association of the R620W polymorphism of protein tyrosine phosphatase PTPN22 with human SLE,” The American Journal of Human Genetics, vol. 75, no. 3, pp. 504–507, 2004. View at Publisher · View at Google Scholar · View at Scopus
  66. C. Vandiedonck, C. Capdevielle, M. Giraud et al., “Association of the PTPN22R620W polymorphism with autoimmune myasthenia gravis,” Annals of Neurology, vol. 59, no. 2, pp. 404–407, 2006. View at Publisher · View at Google Scholar · View at Scopus
  67. I. Cantón, S. Akhtar, N. G. Gavalas et al., “A single-nucleotide polymorphism in the gene encoding lymphoid protein tyrosine phosphatase (PTPN22) confers susceptibility to generalised vitiligo,” Genes and Immunity, vol. 6, no. 7, pp. 584–587, 2005. View at Publisher · View at Google Scholar · View at Scopus
  68. P. Jagiello, P. Aries, L. Arning et al., “The PTPN22 620W allele is a risk factor for Wegener's granulomatosis,” Arthritis & Rheumatism, vol. 52, no. 12, pp. 4039–4043, 2005. View at Publisher · View at Google Scholar · View at Scopus
  69. A. B. Begovich, S. J. Caillier, H. C. Alexander et al., “The R620W polymorphism of the protein tyrosine phosphatase PTPN22 is not associated with multiple sclerosis,” The American Journal of Human Genetics, vol. 76, no. 1, pp. 184–187, 2005. View at Publisher · View at Google Scholar · View at Scopus
  70. B. D. Juran and K. N. Lazaridis, “Update on the genetics and genomics of PBC,” Journal of Autoimmunity, vol. 35, no. 3, pp. 181–187, 2010. View at Publisher · View at Google Scholar · View at Scopus
  71. A. Skórka, T. Bednarczuk, E. Bar-Andziak, J. Nauman, and R. Ploski, “Lymphoid tyrosine phosphatase (PTPN22/LYP) variant and Graves' disease in a Polish population: association and gene dose-dependent correlation with age of onset,” Clinical Endocrinology, vol. 62, no. 6, pp. 679–682, 2005. View at Publisher · View at Google Scholar · View at Scopus
  72. Y. Ban, T. Tozaki, M. Taniyama, M. Tomita, and Y. Ban, “The codon 620 single nucleotide polymorphism of the protein tyrosine phosphatase-22 gene does not contribute to autoimmune thyroid disease susceptibility in the Japanese,” Thyroid, vol. 15, no. 10, pp. 1115–1118, 2005. View at Publisher · View at Google Scholar · View at Scopus
  73. M. C. Totaro, B. Tolusso, V. Napolioni et al., “PTPN22 1858C > T polymorphism distribution in europe and association with rheumatoid arthritis: case-control study and meta-analysis,” PLoS ONE, vol. 6, no. 9, Article ID e24292, 2011. View at Publisher · View at Google Scholar · View at Scopus
  74. C. Capelli, V. Onofri, F. Brisighelli et al., “Moors and Saracens in Europe: estimating the medieval North African male legacy in southern Europe,” European Journal of Human Genetics, vol. 17, no. 6, pp. 848–852, 2009. View at Publisher · View at Google Scholar · View at Scopus
  75. J. J. Just, “Genetic predisposition to HIV-1 infection and acquired immune deficiency virus syndrome: a review of the literature examining associations with HLA,” Human Immunology, vol. 44, no. 3, pp. 156–169, 1995. View at Publisher · View at Google Scholar · View at Scopus
  76. T. Yanagawa, A. Mangklabruks, Y.-B. Chang et al., “Human histocompatibility leukocyte antigen-DQA10501 allele associated with genetic susceptibility to Graves' disease in a caucasian population,” The Journal of Clinical Endocrinology & Metabolism, vol. 76, no. 6, pp. 1569–1574, 1993. View at Google Scholar · View at Scopus
  77. D. Inoue, K. Sato, M. Maeda et al., “Genetic differences shown by HLA typing among Japanese patients with euthyroid Graves' ophthalmopathy, Graves' disease and Hashimoto's thyroiditis: genetic characteristics of euthyroid Graves' ophthalmopathy,” Clinical Endocrinology, vol. 34, no. 1, pp. 57–62, 1991. View at Publisher · View at Google Scholar · View at Scopus
  78. K. Badenhoop, P. G. Walfish, H. Rau et al., “Susceptibility and resistance alleles of human leukocyte antigen (HLA) DQA1 and HLA DQB1 are shared in endocrine autoimmune disease,” The Journal of Clinical Endocrinology & Metabolism, vol. 80, no. 7, pp. 2112–2117, 1995. View at Google Scholar · View at Scopus
  79. H. Tamai, A. Kimura, R.-P. Dong et al., “Resistance to autoimmune thyroid disease is associated with HLA-DQ,” The Journal of Clinical Endocrinology & Metabolism, vol. 78, no. 1, pp. 94–97, 1994. View at Publisher · View at Google Scholar · View at Scopus
  80. C. Cappelli, E. Gandossi, M. Castellano et al., “Prognostic value of thyrotropin receptor antibodies (TRAb) in Graves' disease: a 120 months prospective study,” Endocrine Journal, vol. 54, no. 5, pp. 713–720, 2007. View at Publisher · View at Google Scholar · View at Scopus
  81. M. J. Simmonds, O. J. Brand, J. C. Barrett, P. R. Newby, J. A. Franklyn, and S. C. L. Gough, “Association of Fc receptor-like 5 (FCRL5) with Graves' disease is secondary to the effect of FCRL3,” Clinical Endocrinology, vol. 73, no. 5, pp. 654–660, 2010. View at Publisher · View at Google Scholar · View at Scopus
  82. J. Yang, Q. Qin, N. Yan et al., “CD40 C/T−1 and CTLA-4 A/G49 SNPs are associated with autoimmune thyroid diseases in the Chinese population,” Endocrine, vol. 41, no. 1, pp. 111–115, 2012. View at Publisher · View at Google Scholar · View at Scopus
  83. M. Li, H. Sun, S. Liu et al., “CD40 C/T-1 polymorphism plays different roles in Graves' disease and Hashimoto's thyroiditis: a meta-analysis,” Endocrine Journal, vol. 59, no. 12, pp. 1041–1050, 2012. View at Publisher · View at Google Scholar · View at Scopus
  84. A. A. Zeitlin, J. M. Heward, P. R. Newby et al., “Analysis of HLA class II genes in Hashimoto's thyroiditis reveals differences compared to Graves' disease,” Genes and Immunity, vol. 9, no. 4, pp. 358–363, 2008. View at Publisher · View at Google Scholar · View at Scopus
  85. K. Badenhoop, G. Schwarz, P. G. Walfish, V. Drummond, K. H. Usadel, and G. F. Bottazzo, “Susceptibility to thyroid autoimmune disease: molecular analysis of HLA-D region genes identifies new markers for goitrous Hashimoto's thyroiditis,” The Journal of Clinical Endocrinology & Metabolism, vol. 71, no. 5, pp. 1131–1137, 1990. View at Publisher · View at Google Scholar · View at Scopus
  86. Y. Shi, M. Zou, D. Robb, and N. R. Farid, “Typing for major histocompatibility complex class II antigens in thyroid tissue blocks: association of Hashimoto's thyroiditis with HLA-DQA0301 and DQB0201 alleles,” The Journal of Clinical Endocrinology & Metabolism, vol. 75, no. 3, pp. 943–946, 1992. View at Google Scholar · View at Scopus
  87. G. Barbesino, Y. Tomer, E. Concepcion et al., “Linkage analysis of candidate genes in autoimmune thyroid disease: 1. Selected immunoregulatory genes,” The Journal of Clinical Endocrinology & Metabolism, vol. 83, no. 5, pp. 1580–1584, 1998. View at Publisher · View at Google Scholar · View at Scopus