Endocrine Abstracts

Introduction: Hashimoto’s thyroiditis (HT) is multifactorial disease, caused by a complex interplay of genetic, hormonal, and environmental influences that provoke the development of inappropriate immune responses against thyroid on multiple levels and the initiation of a long-standing autoimmune reaction. Interaction between cellular and humoral immunity is base of HT’s pathogenesis. Our research focuses on the functional activity and the quantity of T regulatory and B regulatory lymphocytes in blood from patients, who have features of HT. A more accurate understanding of role of regulatory cells in the immunotolerance disorders could be a base for the development of new prognostic markers and therapeutic strategies in the treatment of patients with HT.

Main part: We analyzed amount and functional activity subsets of regulatory T and B cells (CD3hiIL-10hi and CD19hiCD38hiCD24hi) in subjects’s blood: patient with isolated hypothyroidism in the outcome of HT (n=23), carriers of antibodies to thyroid tissues (n= 18), patients with HT as a part of autoimmune polyglandular syndrome (APS) (n= 20), healthy donors (HD) (n=13). We found significant differences in the amount of regulatory cells (CD19hiCD38hiD24hi B reg) during in vitro incubation without additional activation in groups carriers of antibodies (1.75% vs 3.0%; P=0.0003) and in groups patients with HT as part of APS (1.5% vs 3.0% P=0.0002) as compared with HD. A decrease in the induction of regulatory B cells was found only in the group of patients with HT as part of APS (2.3%, P=0.04)

Conclusion: Our research has shown that carriers of autoantibodies and patients with HT as part of APS have reduced spontaneous activation of regulatory B cells in vitro and the latter has activation-induced induction of regulatory B cells in the comparison with HD. The quantity and induction of IL-10-producing T cells in the compared groups weren’t significantly differ. The study is supported by the Russian Science Foundation, Grant No.22-15-00135