T cells in autoimmune thyroid disease and pregnancy: an emerging immunological interface

Pregnancy is a condition that requires highly coordinated immunological adaptations to ensure maternal-fetal tolerance while preserving effective immune defense. Among adaptive immune cells, T lymphocytes play a central role in regulating the balance between immune activation and immune tolerance throughout gestation. Distinct T-cell subsets-including T helper (Th)1, Th2, Th17, regulatory T (Treg), and T follicular helper (Tfh) cells-contribute to the dynamic immune changes necessary for a successful pregnancy. Autoimmune thyroid disease (AITD), encompassing Hashimoto's thyroiditis and Graves' disease, is characterized by dysregulated T-cell-mediated immune responses, including enhanced Th1 and Th17 activity and impaired Treg-mediated immune regulation. As AITD frequently affects women of reproductive age, the interaction between AITD and pregnancy-related immune adaptation represents a clinical and immunological challenge. Increasing evidence suggests that persistent immune dysregulation may contribute to thyroid dysfunction and adverse pregnancy outcomes, including pregnancy loss, preterm birth, preeclampsia, and fetal growth restriction. This review summarizes current evidence on T-cell-mediated immune regulation in normal pregnancy and AITD, with particular emphasis on the immunological interactions between these conditions. We discuss physiological changes in major T-cell subsets during pregnancy, mechanisms of immune dysregulation in AITD, and their potential implications for maternal and fetal outcomes. The potential roles of T-cell memory and postpartum immune changes are also briefly considered. A better understanding of T-cell dynamics at the intersection of pregnancy and thyroid autoimmunity may provide further insight into underlying immunological mechanisms and, with further validation, potentially inform future approaches to risk stratification and individualized management.