Akademik Veri Yönetim Sistemi
16th National and 2nd International Congress of Histology and Embryology, Sakarya, Türkiye, 26 Eylül 2024 - 28 Ocak 2025, ss.145-146, (Tam Metin Bildiri)
Introduction: Maternal hypothyroidism is defined as a deficiency of thyroid hormones during pregnancy and affects 4% of the population. Thyroid hormone deficiency during pregnancy influences the health of both the mother and the fetus. Thyroid hormones are crucial for the healthy development and neurodevelopment of the fetus, and their deficiency is well known to cause neurological developmental problems. These hormones reach the fetus via the placenta, and thyroid hormones play an active role in placental tissue throughout pregnancy. They are significant in the proliferation and differentiation of placental cells, and their deficiency has been shown to disrupt the anti-inflammatory environment in the placenta. The disruption of this anti-inflammatory environment leads to the impairment of maternal-fetal immune tolerance, which negatively affects maternal and fetal health by causing various pregnancy pathologies such as preterm birth, miscarriages, and preeclampsia. Maternal immune tolerance is essential for the maternal tissue's acceptance of the semi-allogeneic fetus. The establishment and maintenance of this tolerance depend on an active maternal immune tolerance state mediated by regulatory T cells (Tregs). Treg cells are a subgroup of T cells responsible for balancing excessive immune responses and controlling autoimmunity. Tregs are characterized by CD4, CD25, and FoxP3 (Forkhead family transcription factor forkhead box p3), and a deficiency in FoxP3 expression impairs their functions. In many pregnancy-related pathologies, a reduction in Treg cell populations has been observed. It is known that the release of exosomes increases under pathological conditions. Furthermore, exosomes have been shown to influence the proliferation and differentiation of Treg cells. However, the behavior of Tregs and exosomes in the placenta under conditions of maternal hypothyroidism remains unknown.
Objective: In this study, we aimed to investigate the distribution and concentration of FoxP3+ Treg cells and exosomes in healthy and hypothyroid placentas.
Method: In human placental tissues, Treg cells and exosomes were labeled using FoxP3 and CD63 antibodies, respectively, through immunohistochemistry (IHC). The distribution of Treg cells in the decidua and exosomes in the villi was determined. For quantitative analysis, the expression levels of FoxP3 and CD63 were compared between healthy and patient groups using ELISA. Additionally, histomorphological changes in the placentas were evaluated between these two groups.
Results: IHC results showed a significant decrease in FoxP3 immunoreactivity in hypothyroid placentas compared to the control. Similarly, ELISA results supported the IHC findings.