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The STUDIA UNIVERSITATIS BABEŞ-BOLYAI issue article summary
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Abstract: Hashimoto’s thyroiditis is a human organ-specific autoimmune disease that affects people of all ages, with peak occurrence in women of 30-50 years of age. Chikens of the Obese strain (OS) develop, with high frequency, spontaneous autoimmune thyroiditis (SAT) characterized by circulating antibodies to autologous thyroglobin, infiltration of the thyroid gland with mononuclear cells. The early, predictable onset of SAT on OS chickens provides a unique opportunity to analyse the mechanisms initiating autoimmunity which is virtually impossible to obtain in human. All chikens from this strain develop symptoms of hypothyroidism due to SAT, and the immune system has been shown to be involved in the development of SAT. OS chickens exhibit general immune system hyperactivity, believed in part to be due to intrinsic production of cytokines. Some authors have postulated viral or bacterial infection with proteins similar to a thyroid protein, which may result in activation of thyroid-specific T cells. The evidence for an infectiouse agent as a cause of this disease, however is not convincing. The alternative hypothesis is that the thyroid epithelial cells present their own intracellular proteins to helper T cells. Once activated helper T cells (CD4) may attract other inflammatory cells to the thyroid. The effector mechanism involved in thyroid limphocytic infiltration have been studied, but no definitive concept has yet emerged. Therefore, our studies tried to establish the histological, ultrastructural and immunohistochemical modifications of thyroid gland, and the cellular componants of the thyroid infiltrations in fowl with autoimmune thyroiditis.
Keywords: dendritic cells, lymphocytes, macrophages, plasmocytes.
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