Decreasing secretion of antibodies during intensification of autoimmune process in thyroid gland of comorbidic to chronic inflammation of prostate

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dc.contributor.authorBayraktar, Vasyl M.en
dc.contributor.authorБайрактар, Василь Миколайовичuk
dc.date.accessioned2025-06-13T17:06:52Z
dc.date.available2025-06-13T17:06:52Z
dc.date.issued2025
dc.description.abstractFirst stage of autoimmunization involves the accumulation of macrophages and dendritic cells, as well as plasma cells. In the second stage, the mutual interactions of individual cells in the immune system lead to a decrease in the level of CD8+ in favor of CD4+ , which intensifies the synthesis of T - lymphocyte derivatives, especially Th1, Th17, Tfh, and Tc, reducing the level of Treg. Consequently, the number of the anti-inflammatory cytokines IL-10 and IL-2 decreases, and the synthesis of the pro-inflammatory cytokines IL-2, IL-12, IL-17, IL-21, IL-22, IFN-γ, and TNF-α increases. The latter two especially trigger the pyroptosis process involving the inflammasome. Activation of the inflammasome by IL-β and IL-18 produced by macrophages is one of the mechanisms of pyroptosis in the course of Hashimoto’s thyroiditis, involving Gram-negative bacteria and NLRC4. In the next step, the apoptosis of thyroid cells is initiated by the intensification of perforin, granzyme, and proteoglycan synthesis by Tc and NK cells. Sufferers with Hashimoto’s thyroiditis may experience thyroid damage and hypothyroidism, which manifests with elevated levels of thyroid-stimulating hormone (TSH) and decreased levels of free thyroxine (T4) and free triiodothyronine (T3) in the blood. Sufferes with subclinical hypothyroidism are at increased risk of cardiovascular disease. Properly managed thyroid hormone replacement therapy significantly improves sufferer's health status and reduces the risk of heart attack, stroke, arrhythmia, heart failure, or cardiovascular-related death. It should be emphasized that sufferers with Hashimoto’s thyroiditis (HT) are more likely to develop both cancerous and non-cancerous changes. Furthermore, a significant increase in the risk of cardiovascular events and cardiovascular-related mortality has been demonstrated in sufferers with a thyroid-stimulating hormone (TSH) level of 10 mIU/mL or higher. The presence of an autoimmune disease in a sufferers increases the risk of subsequent diseases resulting from auto-aggression. This is due to abnormal humoral and cellular responses to self-antigens.en
dc.identifier.citationBayraktar V. M. Decreasing secretion of antibodies during intensification of autoimmune process in thyroid gland of comorbidic to chronic inflammation of prostate / V. M. Bayraktar // Українська школа ендокринології : матеріали наук.-практ. конф. (Харків, 5–6 черв. 2025 р.). – Харків : ДУ ІПЕП, 2025. – С. 11–15.en
dc.identifier.urihttps://dspace.onu.edu.ua/handle/123456789/41690
dc.language.isoen
dc.publisherІнститут проблем ендокринної патології ім. В. Я. Данилевського Національної академії медичних наук Україниuk
dc.subjectthyrozolen
dc.subjecttiiodothyronineen
dc.subjectlevothyroxineen
dc.subjectthyroid glanden
dc.subjectL-selenmethionineen
dc.subjectL-thyroxinen
dc.subjectHashimoto’s thyroiditisen
dc.subjectthyroid microsomal antibodies (TPO-Ab)en
dc.titleDecreasing secretion of antibodies during intensification of autoimmune process in thyroid gland of comorbidic to chronic inflammation of prostateen
dc.typeArticleen
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