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International Journal of Endocrinology
Volume 2015 (2015), Article ID 747816, 9 pages
Review Article

Cytotoxic T Lymphocyte-Associated Antigen 4 Gene Polymorphisms and Autoimmune Thyroid Diseases: An Updated Systematic Review and Cumulative Meta-Analysis

1School of Public Health, Taishan Medical University, Taian 271000, China
2School of Basic Medical Sciences, Taishan Medical University, Taian 271000, China
3Ruijin Hospital, Shanghai Jiao Tong University, Shanghai 200025, China
4School of Public Health, Shandong University, Jinan 250012, China

Received 16 January 2015; Accepted 17 February 2015

Academic Editor: Maria L. Dufau

Copyright © 2015 Hai-Feng Hou 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.


The association of the cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) gene and susceptibility to autoimmune thyroid diseases (AITDs) has been studied extensively. However, the results were not the same in different ethnic groups. We updated the meta-analysis of association of CTLA-4 gene polymorphisms with AITDs and summarized the results in specific ethnicity. The associations of A49G gene polymorphism with GD, A49G gene polymorphism with HT, CT60 gene polymorphism with GD, and CT60 gene polymorphism with HT were summarized based on the literatures published up to October 30, 2014, in English or Chinese languages. The participants involved in the studies of A49G with GD, A49G with HT, CT60 with GD, and CT60HT were 39004 subjects (in 51 studies), 13102 subjects (in 22 studies), 31446 subjects (in 22 studies), and 6948 subjects (in 8 studies), respectively. The pooled ORs of CTLA-4 gene polymorphisms with AITDs were larger than 1.00, and the 95% CIs of ORs were statistically significant among whole population analyses. However, the subgroup analysis demonstrated that pooled ORs of A49G polymorphisms with GD among Africans or Americans are less than 1.00. The accumulated evidence suggests that the G allele mutant of A49G and CT60 increased the risks of HT and GD.