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pubmed:abstractText |
Experimental autoimmune thyroiditis (EAT) in mice is characterized by production of anti-thyroglobulin autoantibodies and lymphoid infiltration of the thyroid gland. The pathogenesis of EAT is genetically controlled, but its mechanism is not yet clear. To investigate the mode of the expression of genetic control in the development of the disease, we attempted to modulate immune responses with thymosin fraction 5 (T-5) in mice which are either high or low responders to thyroglobulin. Severe thyroid lesions in high responder mice appear 2-3 weeks after immunization, while low responders develop very mild or no lesions. High responder mice have also higher antibody titer than the low responder strain. T-5 administered in five daily injections before or simultaneously with immunization, was strongly suppressive to EAT development in the high responder strain while there was no effect on thyroiditis level in low responder mice. T-5 also decreased the severity of thyroiditis in high responder mice when injected 2-4 weeks after immunization. In low responder mice, however, the same treatment increased the thyroiditis level. The effects of late injection of T-5 were dose-dependent. In all experiments, the antibody titres were not affected by T-5 treatment. The results demonstrate the ability of T-5 to modulate development and intensity of EAT. The contrasting effects of T-5 in high and low responder mice illustrate the relationship between the effects of T-5 and host immune status prior to study, suggesting that the level of immunoregulatory cell activity may differ in these two strains.
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