Upregulation of thyroid transcription factor-1 and human leukocyte antigen class I in Hashimoto's disease providing a clinical evidence for possible triggering autoimmune reaction

ObjectiveAn increase in the expression of autoantigens and their presenting molecules human leukocyte antigen (HLA) class I has been demonstrated to be responsible for autoimmune diseases. Thyroid transcription factor-1 (TTF-1 or NKX2-1) synchronously upregulates both HLA class I and thyroid-specifi...

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Published inEuropean journal of endocrinology Vol. 164; no. 5; pp. 795 - 800
Main Authors Huang, Huibin, Li, Xisheng, Lin, Ling, Shi, Yaxiong, Lin, Xiahong, Li, Liangyi, Xu, Dongming
Format Journal Article
LanguageEnglish
Published Bristol BioScientifica 01.05.2011
European Society of Endocrinology
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Summary:ObjectiveAn increase in the expression of autoantigens and their presenting molecules human leukocyte antigen (HLA) class I has been demonstrated to be responsible for autoimmune diseases. Thyroid transcription factor-1 (TTF-1 or NKX2-1) synchronously upregulates both HLA class I and thyroid-specific autoantigen, which may be involved in the pathological process of autoimmune thyroiditis. In this study, the expressions and potential role of TTF-1 and HLA class I in Hashimoto's disease (HT) were examined.PatientsIn this study, 22 resection specimens clinically and histopathologically confirmed to have Hashimoto's disease and 30 normal thyroid specimens from adjacent tissues of thyroid adenoma were used.MeasurementWestern blot, real-time PCR, and immunohistochemistry were performed to assay TTF-1 and HLA class I in the thyrocytes of Hashimoto's disease as well as in the normal thyroid from adjacent tissues of thyroid adenoma.ResultsThe TTF-1 and HLA class I in Hashimoto's disease were significantly higher than those in the controls.ConclusionUpregulation of TTF-1 and HLA class I in Hashimoto's disease provide a clinical evidence for possible triggering of autoimmune reaction.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
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ISSN:0804-4643
1479-683X
1479-683X
DOI:10.1530/EJE-10-0960