摘要：

Chickens of the Obese strain (OS) develop a spontaneous, hereditary autoimmune thyroiditis during the first weeks of life which parallels human Hashimoto's thyroiditis in all clinical, histopathological and serological aspects. This review summarizes the results from investigations on this strain with special emphasis on the pathogenic effector mechanisms leading to the autoimmune destruction of the thyroid gland. The fact that this model disease arises in an avian species is particularly advantageous because of the clear-cut anatomical and functional division of the immune system. Data are discussed which suggest the following pathogenesis of spontaneous autoimmune thyroiditis: B cells and their products, i.e. thyroglobulin autoantibodies, play a decisive role in the initial phases of the disease, such antibodies are first vertically transferred from the mother hen via the egg yolk into the embryo and newly hatched chick, the immune system of which then takes over their production. T-helper cells are required for the formation of the thyroglobulin autoantibodies. These antibodies can either be complement-fixing or mediate destruction of the target cells via antibody-dependent cellular cytotoxicity (ADCC). B cells themselves also destroy thyroid epithelial cells directly in ADCC-like fashion. Cytotoxic T cells seem to play a minor role in the beginning, but add to the destruction of the thyroid gland later. The underlying defect appears to be a deficient intrathymic maturation of suppressor cells leading to a lack of their emigration to the periphery. The development of the disease is under multigenic control, involving at least three loci. Genes associated with the B locus (the major histocompatibility complex (MHC) of the chicken) and a non-B locus seem to be responsible for the immunological hyperreactivity of the OS towards autologous (thyroid and non-thyroid) and exogenous antigens. The third locus is considered to determine a primary thyroid defect thus predisposing this organ as a prime target for the manifestation of autoimmune disease in the OS.

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