Toll-Like Receptors-2 and -4 in Graves' Disease-Key Players or Bystanders?

Agnieszka Polak,Ewelina Grywalska,Jacek Roliński,Maria Klatka,Beata Matyjaszek-Matuszek,Janusz Klatka

doi:10.3390/ijms20194732

Agnieszka Polak, Ewelina Grywalska + Show 4 more

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https://doi.org/10.3390/ijms20194732

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Abstract

Graves’ disease (GD) is an autoimmune disease that affects the thyroid. The development of autoimmunity is associated with innate immune responses where the prominent role plays Toll-like receptors (TLRs). The aim of our study was to assess the relationship between the expression levels of TLR-2 and TLR-4 on CD4+ and CD8+ T as well as CD19+ B lymphocytes in patients with GD and selected clinical parameters. The study group consisted of 32 women with GD, the control group consisted of 20 healthy women. Immunophenotyping was performed using the flow cytometry and cytokines concentrations were assessed using ELISA assay. The mean percentage of CD4+/TLR-2+ and CD8+/TLR-2+ T cells in patients with GD was higher than in the control group (p < 0.0001). After obtaining euthyroidism, the mean percentage of CD4+/TLR-2+ T cells in patients with GD decreased (p < 0.0001). The expression level of TLR-2 on CD4+ T lymphocytes correlated with serum FT3 concentration in patients with GD (r = 0.47, p = 0.007). The mean percentage of CD8+/TLR-2+ T cells in patients with GD before treatment compared to patients with GD after obtaining euthyroidism was higher (p = 0.0163). Similar findings were found for TLR-4. Thus the TLR-2 and TLR-4 can be a prognostic marker for Graves’ disease.

Highlights

Graves’ disease (GD) is an autoimmune thyroid disease with complex and incompletely established etiology
structure parameter inference approach (SPINA)-GD was significantly increased in patients with GD before treatment, and it decreased to near normal values when the patients became euthyroid (Table 2)
The mean Jostel’s THSK Index (JTI) was negative in patients with GD, and it decreased further after thyrostatic treatment (Table 2)

Summary

Introduction

Graves’ disease (GD) is an autoimmune thyroid disease with complex and incompletely established etiology It may occur in genetically predisposed individuals who are exposed to certain exogenous factors, such as iodine, selenium, smoking, bacterial and viral infections, allergies, radiotherapy or emotional stress. GD develops due to a loss of immunological tolerance and reactivity to thyroid autoantigens, mainly directed against the thyrotropin receptor. This leads to the infiltration of this gland by T lymphocytes and B lymphocytes that produce antibodies specific for this disease entity, with a clinical manifestation of hyperthyroidism in the form of GD [1,2,3,4]. In view of the disturbing increase in the incidence rate of GD, hyperthyroidism with an autoimmune background has become an important health problem [5]

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