Abstract

Thyroid orbitopathy (OT), as an organ‑specific autoimmune disease, is a result of immune dysregulation leading to loss of control over inflammation directed against self‑antigens. The source of the autoreactive lymphocytes is the impairment of central tolerance as well as their induction on the periphery by modified or sequestered by that time antigens. Active suppression by the various subpopulations of regulatory lymphocytes (Lreg) acts as a counterbalance to the proinflammatory factors and is aimed at dampening pathological reaction. Thereby, qualitative or quantitative shortfalls of Lreg play a critical role in the development of autoimmune diseases. Giving direction to Lreg‑based therapy and restoring the dynamic balance seem to be of crucial importance, especially in diseases such as OT, where the causative self‑antigen is not yet unequivocally elucidated.Technical difficulties with isolation and assessment of Lreg function in vitro as well as lack of unification of research protocols make the findings non‑comparable, inconclusive and sometimes even conflicting. Lack of a Tregs’ (regulatory T cells) specific set of surface markers makes the demethylation status analysis of TSDR (Treg specific demethylated region) FOXP3 (forkhead box P3) locus the most reliable method of their quantification. Despite numerous discrepancies between research findings, most of them point to Lreg’s pivotal role in immune disturbances, which form the basis of OT and autoimmune thyroid diseases (AITD).

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