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Common Allelic Variants of Exons 10, 12, and 33 of the Thyroglobulin Gene Are Not Associated with Autoimmune Thyroid Disease in the United Kingdom

Division of Medical Sciences, University of Birmingham, Institute of Biomedical Research (J.E.C., J.M.H., H.F., J.C.-S., J.A.F., S.C.L.G.), Birmingham B15 2TT, United Kingdom; Juvenile Diabetes Research Foundation/Wellcome Trust Diabetes and Inflammation Laboratory, Cambridge Institute for Medical Research, University of Cambridge (J.M.M.H.), Cambridge CB2 2XY, United Kingdom; and Division of Medical Sciences, University of Birmingham, Heartlands Hospital (S.C.L.G.), Birmingham B9 5SS, United Kingdom

Address all correspondence and requests for reprints to: Dr. S. C. L. Gough, Department of Medicine, University of Birmingham, Heartlands Hospital, Bordesley Green East, Birmingham, United Kingdom B9 5SS. E-mail: s.c.gough{at}bham.ac.uk.

Thyroglobulin (Tg) is a major autoantigen for autoimmune thyroid disease (AITD). The Tg gene (Tg) has been mapped to chromosome 8q24, which has recently been linked in two independent studies to AITD. Association of specific alleles of microsatellite markers within Tg itself supports a role for Tg as a good candidate susceptibility locus for AITD. Resequencing of the Tg exons has led to the identification of a number of novel single nucleotide polymorphisms, four of which have been reported to be associated with AITD. Resequencing of Tg in Caucasian subjects in the United Kingdom (UK) has confirmed the presence of four single nucleotide polymorphisms in exons 10, 12, and 33. However, in the largest case-control association study to date with adequate power to detect the reported effect if present, we found no evidence for association of the Tg DNA variants with AITD in the UK. These data suggest that the recently identified single nucleotide polymorphisms do not have a causal role for AITD in the UK. At this stage, we cannot exclude the Tg region as harboring a susceptibility locus for AITD, and only large scale sequencing and fine mapping of the region, including neighboring genes, will allow us to identify any potential causal variants within this region.

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