Article
Infiltrating Th1/Th17 cells predominate in Hashimoto’s Thyroiditis
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Published: | April 24, 2015 |
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Introduction: Hashimoto’s thyroiditis (HT) is an autoimmune thyroid disease characterized by lymphocyte infiltration, fibrosis, and parenchymal atrophy of the thyroid gland. However, little is known about the role of infiltrating T-cells in the etiopathogenesis of HT. The aim of the study was to characterize the phenotype and function of isolated T cells (Th1, Th17 versus regulatory T cells, Tregs) from the thyroid gland.
Material and methods: Thyroid tissue and peripheral blood mononuclear cells (PBMCs) were obtained from seven HT patients who underwent thyroidectomy. After in vitro expansion, the cytokine production profiles of isolated infiltrating T-cells and PBMCs were assessed by flow cytometry following unspecific stimulation. Cell surface markers, chemokine-ligand 20 (CCL20) and Treg transcription factor FoxP3 were analyzed by immunohistochemistry.
Results: Infiltrating cells were mostly CD4 T-cells with a predominant memory-effector phenotype CD4 CD45RO CD27 . Infiltrating CD4 T-cells up-regulated the expression of chemokine-receptors CCR5 (5.5%), CCR6 (9.6%) and CXCR3 (9.3%), producing high amounts of IFNgamma (41.3%) and IL-17 (4.0%) compared to circulating CD4 T-cells. High numbers of CD4 CD25 CD127-FoxP3 (Tregs) were found in infiltrating cells (2.9%) compared to peripheral blood. Immunohistological analysis of the thyroid gland demonstrated the abundance of CD4 CD45RO CD27 T-cells, the expression of CCL20 and expression of FoxP3.
Conclusion: Our findings suggest that infiltrating T-cells, possibly driven by chemokine-receptors, belong to the Th1/Th17 effector T-cell phenotype producing high amounts of IFNgamma and IL-17. The presence of Tregs within inflammatory tissue may indicate a role of these cells in modulating inflammation, but it has to be proven whether infiltrating Tregs are functionally active on suppression of Th1/Th17 responses.