title: 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.
abstract: OBJECTIVE
  An 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.
  
  
  METHODS
  In 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.
  
  
  METHODS
  Western 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.
  
  
  RESULTS
  The TTF-1 and HLA class I in Hashimoto's disease were significantly higher than those in the controls.
  
  
  CONCLUSIONS
  Upregulation of TTF-1 and HLA class I in Hashimoto's disease provide a clinical evidence for possible triggering of autoimmune reaction.
authors.affiliation: Second Affiliated Hospital of Fujian Medical University, Quanzhou, People's Republic of China.
authors.forename: Huibin
authors.initials: H
authors.lastname: Huang
authors.forename: Xisheng
authors.initials: X
authors.lastname: Li
authors.forename: Ling
authors.initials: L
authors.lastname: Lin
authors.forename: Yaxiong
authors.initials: Y
authors.lastname: Shi
authors.forename: Xiahong
authors.initials: X
authors.lastname: Lin
authors.forename: Liangyi
authors.initials: L
authors.lastname: Li
authors.forename: Dongming
authors.initials: D
authors.lastname: Xu
mesh_terms: D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000096:biosynthesis; D005260:Female; D006680:HLA Antigens / Q000096:biosynthesis* / Q000276:immunology; D050031:Hashimoto Disease / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D015395:Histocompatibility Antigens Class I / Q000096:biosynthesis* / Q000276:immunology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009687:Nuclear Proteins / Q000096:biosynthesis* / Q000502:physiology; D000074482:Thyroid Nuclear Factor 1; D014157:Transcription Factors / Q000096:biosynthesis* / Q000502:physiology; D015854:Up-Regulation / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D006680:HLA Antigens; D015395:Histocompatibility Antigens Class I; C000614412:NKX2-1 protein, human; D009687:Nuclear Proteins; D000074482:Thyroid Nuclear Factor 1; D014157:Transcription Factors