Abstract
The link between Graves’ disease (GD) and Hashimoto’s thyroiditis (HT) has been debated for decades due to the shared pathological and immunological components. Immune intolerance and inappropriate immune reaction against self-thyroid cells are distinctive features of both diseases, but definitive data for the clinical presentation of autoimmune thyroid disease remains unclear. To analyse the expression of T-regulatory cells, CD58, the CD4/CD8 ratio and the neutrophil/lymphocyte ratio and to determine if these parameters could be used as differentiating markers between auto- and non-immune thyroid diseases, 75 patients were enrolled in this study—40 with autoimmune thyroid disease (HT and GD ), 15 with non-immune thyroid disease, and 20 healthy controls. Multicolour flow cytometry was used to analyse CD58, T-regulatory cells (Treg) expressing CD4, CD25, HLA-DR and CD8 using different stained fluorescent labelled monoclonal antibodies. The neutrophils and lymphocyte ratio was also measured. Lower expression of Treg with higher expression of CD58 (LFA-3) was found in the autoimmune diseases when compared with the non-immune and control groups. ROC analysis showed that CD58 with sensitivity 88% and specificity 100% with cut-off value more than or equal to 29.9 indicates Hashimoto’s disease, while lower value indicates colloid goitre, and higher or equal to 29.84 indicates Graves’ disease and lower indicates colloid goitre with 100% sensitivity and specificity. CD58 could be used as differentiating marker between immune and non-immune thyroid disorders.
Highlights
Autoimmune thyroid disease (AITD) is an immunological, clinically heterogeneous, specific organ disease typified by Graves’ disease (GD) is the predominant AITD and is caused by autoantibodies to thyroid-stimulating hormone receptor (TSHR) augmenting its action and inducing thyrotoxicosis; two other autoantibodies, directed to thyroid peroxidase (TPO) and thyroglobulin (Tg), may occur and share classical marker of Hashimoto’s thyroiditis (HT) (Fountoulakis and Tsatsoulis 2004)
Assessment of the expression of lymphocyte functionassociated antigen-3 (LFA-3) was done using CD58-fluorescein isothiocyanate (FITC) (BD Bioscience, 555920), while the expression of T-regulatory cells (Treg) cells was based on number of helper cells CD4 with CD25 (FITC), HLA-DR (APC) (B.D Bioscience, San Jose, CA, USA) and HLA-DR (FITC) (35298)
Thyroid disease was more common in females than males: 88% in HT, 53.3% in GD and 86.7% in colloid goitre (CG)
Summary
Autoimmune thyroid disease (AITD) is an immunological, clinically heterogeneous, specific organ disease typified by GD is the predominant AITD and is caused by autoantibodies to thyroid-stimulating hormone receptor (TSHR) augmenting its action and inducing thyrotoxicosis; two other autoantibodies, directed to thyroid peroxidase (TPO) and thyroglobulin (Tg), may occur and share classical marker of HT (Fountoulakis and Tsatsoulis 2004). GD may exhibit mild lymphocytic thyroiditis and progress to hypothyroidism with clinical manifestation similar to HT (Ehlers et al 2012). Clinical presentation of both diseases may overlap with non-immune colloid goitres and present problems with regard to diagnosis, even requiring invasive techniques such as fine needle aspiration or even biopsy to reach the final diagnosis. Comp Clin Pathol (2018) 27:721–727 the pathophysiological relationship between TSHR, TPO and Tg autoantibodies remains uncertain (McLachlan et al 2007). Both GD and HT show thyroid lymphocytic infiltration which suggests the possibility of similar underlying pathogenesis. The complex interaction between genetic susceptibility and environmental factors initiating this process, and loss of immunological tolerance at multiple levels, explains how this interaction operates (Dantus 2008; Tomer 2010)
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