200
Views
12
CrossRef citations to date
0
Altmetric
Full-Length Research Paper

Polymorphisms in TLR1, TLR6 and TLR10 genes and the risk of Graves’ disease

, , , , , , & show all
Pages 13-18 | Received 14 Mar 2014, Accepted 22 Jun 2014, Published online: 16 Jul 2014
 

Abstract

Graves’ disease (GD) is postulated to be caused by the combined effects of susceptibility genes and environmental triggers. Toll-like receptors (TLRs) play a role in the activation of innate and adaptive immune responses in mammalians. The aim of this study was to evaluate the potential association of polymorphisms in TLR1, TLR6 and TLR10 genes with GD in Chinese Cantonese population. Seven single nucleotide polymorphisms (i.e. rs4833095 and rs5743565 in TLR1; rs5743808 in TLR6; and rs4504265, rs11466655, rs11096957 and rs10856839 in TLR10) were evaluated in 332 GD patients and 351 unrelated controls from Chinese Cantonese population. SNP rs5743565 in TLR1 conferred a protective effect against GD. The minor allele G of rs5743565 decreased the risk of GD in all cases (odds ratio; ORG vs. A = 0.72 (0.58–0.91); p = 0.005; ptrend = 0.004) and early onset patients (ORG vs. A = 0.72 (0.56–0.91); p = 0.007; ptrend = 0.006). This study provided evidence that genetic variation rs5743565 in TLR1 might be associated with the decreased susceptibility of GD.

Acknowledgements

We gratefully acknowledge Ms. Yan Tai (The Third Affiliated Hospital of Sun Yat-sen University) for technical assistance.

Declaration of interest

None of the authors has any potential financial conflict of interest related to this manuscript. The authors alone are responsible for the content and writing of this article.

This work was funded by the Fundamental Research Funds for the Central Universities (21614333), the project of Guangdong Natural Science Foundation (No. 8151063201000) and the “Program for New Century Excellent Talents in Universities” (NCET-05-0745).

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.