Endocrine Abstracts

Considering, the pivotal role of DC in formation and development of autoimmunological processes, the investigation of influence of of thyrometabolic status on maturation and function of subtypes of human peripheral blood DC, seems to be reasonable and of particular interest. THE AIM of the present study was a complex analysis of the dendritic cell subsets and fenotypes in patients with chronic thyroiditis (ChT) as well as the patients monitored for differentiated thyroid cancer (DTC).

Patients and methods: Blood samples were collected from patients suffering from ChT before and after treatment with L-T₄ (N=18). Moreover, to investigate the influence of thyroid hormones, blood samples for ex vivo analysis were collected from thyroidectomised (because of differentiated thyroid carcinoma) patients (n=21) at two time points: (i) after withdrawal of L-T4 treatment group before treatment, and (ii) during 2 months of L-T4 administration in order to suppress TSH concentration group after treatment. FACS analysis of expression of selected molecules on the blood dendritic cells was performed. Furthermore, the investigation of the DC cell culture was performed in the conditions of deficiency and excess of T3.

Results: We found that the percentage of pDCs and mDC in peripheral blood was dependent on thyrometabolic state and that in patients with ChT this regulation was partially impaired. Additionally, we observed lower expression of CD86 on myeloid DCs in hypothyroid ChT patients as compared to thyroidectomised patients. Interestingly this difference was attenuated by L-T₄ treatment. The effect of thyroid hormones on surface expression of co-stimulatory molecules was then confirmed in vitro in experiments with freshly sorted human DCs.

Conclusions: Results of our study indicate that thyroid hormones influence the biology of peripheral blood DCs. This regulatory effect was furthermore affected by chronic thyroiditis. This observation might be of great importance for understanding of immune disorders of endocrine system.