title: HLA-G does not have a pathophysiological role in Graves' disease.
abstract: OBJECTIVE
  It has been suggested that the non-classic HLA class I molecule HLA-G plays a role in autoimmune disease by protecting tissues from damage by infiltrating cytotoxic T cells. Such infiltration occurs in the thyroid of patients with Graves' disease (GD) and Hashimoto's thyroiditis (HT) and can eventually result in tissue destruction. The aim of the current study was to analyse thyroid tissue and thyrocytes obtained from individuals with autoimmune thyroid disease for the expression of HLA-G.
  
  
  METHODS
  HLA-G expression was analysed in thyroid tissue taken from six patients with GD and one with HT by reverse transcriptase polymerase chain reaction. Thyroid tissue samples isolated from six patients with multinodular goitre (MNG) were used as non-autoimmune controls. HLA-G expression was also examined in cultured thyroid follicular cells (TFCs).
  
  
  RESULTS
  The expression of HLA-G was not detected in the thyroid gland of patients with either GD, HT, or MNG. Furthermore, HLA-G expression could not be detected in cultured patient TFCs under basal conditions or after stimulation with the proinflammatory cytokines-interleukin 1alpha, interferon gamma, and tumour necrosis factor alpha.
  
  
  CONCLUSIONS
  HLA-G expression does not occur in the thyroid of patients with GD, indicating that HLA-G does not play a pathophysiological role in this autoimmune disorder. Although the expression of HLA-G was not detected in the thyroid sample of the patient with HT, a greater sample size would be required to conclude that HLA-G does not have a part to play in this autoimmune thyroid disease.
authors.affiliation: Division of Clinical Sciences (North), University of Sheffield, UK. e.h.kemp@sheffield.ac.uk
authors.forename: E H
authors.initials: EH
authors.lastname: Kemp
authors.forename: R A
authors.initials: RA
authors.lastname: Metcalfe
authors.forename: P F
authors.initials: PF
authors.lastname: Watson
authors.forename: A P
authors.initials: AP
authors.lastname: Weetman
mesh_terms: D000199:Actins / Q000378:metabolism; D001327:Autoimmune Diseases / Q000378:metabolism*; D002478:Cells, Cultured; D015870:Gene Expression; D006111:Graves Disease / Q000378:metabolism*; D006680:HLA Antigens / Q000235:genetics / Q000378:metabolism*; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013961:Thyroid Gland / Q000378:metabolism
chemical_list: D000199:Actins; D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I