Immune-Endocrine Interactions in Autoimmune Thyroid Diseases

Abstract

Autoimmune thyroid diseases (AITD) are the most common organ-specific autoimmune disorders affecting approximately 5% of the overall population. An aberrant interaction between abnormal thyrocytes, abnormal antigen-presenting cells and abnormal T cells forms the basis for the atypical autoimmune reaction targeting thyroid antigens. It was proposed that nongenetic (environmental and hormonal) factors play a crucial etiological role in AITD development, through altering immune-endocrine interactions. The most outstanding fact is that in genetically predisposed individuals, the disruption of these neuroendocrine-immune interactions by environmental factors results in thyroid autoimmune dysfunction. These interactions are able to incline the balance between Th1-Th2 immune response toward one side, resulting in a Th1-cell-mediated autoimmune reaction with thyrocyte destruction and hypothyroidism in Hashimoto’s thyroiditis but to a hyperreactive Th2-mediated humoral response against TSH receptor with stimulatory antibodies leading to Graves’ disease hyperthyroidism. In this review the main mechanisms involved are summarized. In this sense, the participation of stress-mediated activation of the sympathoadrenal system and hypothalamic-pituitary-adrenal axis, the hormonal changes occurring during pregnancy and postpartum acting on antigen-presenting cells and influencing, in this way, the balance of the immune status are shown to participate in AITD etiology. The possibility that altered levels of thyroid hormones during the course of the AITD may alter immune function is also discussed.

Thyroid autoimmunity as a window to autoimmunity: An explanation for sex differences in the prevalence of thyroid autoimmunity

“…In addition, the stress disruption of the Hypothalamic-Pituitary-Adrenal (HPA) axis is also seen to play a role in the altering of the immune response characteristics (Klecha et al, 2008).…”

Dysfunction of Maternal Thyroid Hormones and Psychiatric Symptoms

“…Hypothyroidism can cause several abnormalities as the following (Klecha et al, 2000(Klecha et al, & 2006De Vito et al, 2011): (1) increase the levels of reactive oxygen species (ROS); (2) augmentation of phagocytosis; (3) elevate the activities of the proinflammatory markers such as interleukin-1β and macrophage inflammatory protein-1α; (4) decrease the activities of the antioxidant enzymes; (5) reduce the lymphocyte proliferation parameters; (6) diminish the cell migration and the production of antibody; and (7) decrease the immune response. As well, hyperthyroidism can reduce the activities of the proinflammatory markers such as monocytes and macrophages (Klecha et al, 2008;De Vito et al, 2012). According these reports, it is probable that indirect roles of THs via glial cells are significant for the activity of neuronal cells and their defects may at least in part, cause several psychiatric symptoms (Noda, 2015).…”

Selenium and thyroid gland

“…Аутоиммунные тиреопатии (БГ и различные ва рианты АИТ) наиболее распространенные АИЗ, ко торые встречаются не менее чем у 5% населения ми ра, преимущественно у женщин, клинически прояв ляющиеся нарушением функции ЩЖ (гипотиреоз и/или тиреотоксикоз) [43]. Этиология указанных за болеваний недостаточно изучена.…”