HLA-G does not have a pathophysiological role in Graves' disease

Abstract

Aims: 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.

Figure 1

RT-PCR analysis of HLA-G and β actin gene expression in thyroid tissue samples from patients with autoimmune thyroid disease. The cDNA samples were from: fetal chorionic membranes (lane 1); thyroid tissue from a patient with Graves’disease (lane 2); thyroid tissue from a patient with Hashimoto’s thyroiditis (lane 3); thyroid tissue from a patient with multinodular disease (lane 4); and negative control without cDNA (lane 5).

Figure 2

Reverse transcription polymerase chain reaction analysis of HLA-G and β actin gene expression in thyroid cell culture. The cDNA samples were from: HLA-G cDNA in pcDNA3 (lane 1); unstimulated thyroid follicular cells (TFCs) (lane 2); TFCs stimulated with: interleukin 1α (lane 3), interferon γ (IFNγ; lane 4), thyroid stimulating hormone (lane 5), tumour necrosis factor α (TNFα; lane 6) and TNFα plus IFNγ (lane 7); and negative control without cDNA (lane 8).