Abstract
The role of the thymus in the pathogenesis of experimental allergic thyroiditis (EAT) in the guinea pig was studied after the lapse of a sufficiently long period following adult thymectomy. Female Hartley guinea pigs thymectomized or sham-operated at 10 to 12 weeks of age were immunized by a single injection of homologous thyroid extract in complete Freund's adjuvant (CFA) 7 or more months after operation. The animals were sacrificed at 4 or 5 weeks after immunization. Adult thymectomized and subsequently sensitized (ATx-sensitized) animals showed a markedly depressed ability to develop thyroiditis, 18 of the 21 animals having thyroid lesions which could be graded as slight or lower than the sham-operated controls. Delayed skin reaction and macrophage migration inhibitory factor (MIF) production of lymph node cells to thyroid antigen were reduced in the ATx-sensitized animals. On the contrary, enhancement of migration was noted in some of the animals. Anti-thyroid hemagglutinating antibody was not detected in about a quarter of ATx-sensitized animals, in the remainders of which the titers were found to be at the level similar to that of the sham-operated controls. There was a substantial decrease in the percentage of rosette-forming cells (T cells) on unsensitized ATx animals 14 months after operation. Thus, it seems reasonable to conclude that the suppression of the development of thyroiditis and related cellular immunity are a reflection of a decline in peripheral T cell population during the long term after thymectomy, and EAT in the guinea pig is a thymus dependent disease.
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