| Autor: |
Adamska-Fita E; Department of Endocrinology and Metabolic Diseases, Polish Mother's Memorial Hospital-Research Institute, 93-338 Lodz, Poland., Śliwka PW; Department of Endocrinology and Metabolic Diseases, Polish Mother's Memorial Hospital-Research Institute, 93-338 Lodz, Poland.; Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, 93-338 Lodz, Poland., Karbownik-Lewińska M; Department of Endocrinology and Metabolic Diseases, Polish Mother's Memorial Hospital-Research Institute, 93-338 Lodz, Poland.; Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, 93-338 Lodz, Poland., Lewiński A; Department of Endocrinology and Metabolic Diseases, Polish Mother's Memorial Hospital-Research Institute, 93-338 Lodz, Poland., Stasiak M; Department of Endocrinology and Metabolic Diseases, Polish Mother's Memorial Hospital-Research Institute, 93-338 Lodz, Poland. |
| Abstrakt: |
The expression of thyroid-stimulating hormone receptor (TSHR) has been documented on various immune cells, including B lymphocytes, T lymphocytes, Natural Killer (NK) cells, monocytes, and dendritic cells (DCs). Natural Killer T (NKT) cells serve as a crucial link between innate and adaptive immunity, playing significant roles in immunological interactions and autoimmune diseases. The aim of the present study was to evaluate the presence of TSHR on NKT cells. Our research involved patients with thyroid disease, as well as healthy controls. Peripheral blood mononuclear cells (PBMCs) and, thereafter, NKT cells were isolated from 86 patients with benign nodular thyroid disease with and without autoimmune thyroid disease (AITD) (28 and 56 cases, respectively), and TSHR expression was analyzed using fluorescence-activated cell sorting (FACS). In order to confirm the results, the reverse-transcription polymerase chain reaction (RT-PCR) method was used in cells obtained from healthy individuals. Our findings obtained with application of the FACS method revealed that TSHR is not expressed on NKT cells in either AITD or non-AITD patients, though TSHR was detected in the total PBMC population (TSHR+ cells 2.77%). The absence of TSHR on NKT cells was further confirmed with RT-PCR in healthy individuals ( p < 0.0001). These results questioned the previously suggested direct influence of NKT cells on AITD development. |
