In the Cornell C strain of White Leghorn chickens, thyroiditis appeared spontaneously. It was characterized by phenotypic changes due to a decrease of thyroxine, histological damage to the thyroid gland, and the presence in the seruim of antibodies to thyroglobulin. Susceptibility to the disease is genetically inherited. Hormonal bursectomy (androgen given to the embryo) suppresses the development of thyroiditis.
Obese strain chickens develop circulating autoantibodies to thyroglobulin and lymphocytic infiltration of their thyroids during aging. Two alleles, B(1) and B(4), are found with high gene frequency at the major histocompatibility (B) locus. Greater pathology and higher antibody titers are observed in B(1)B(1) and B(1)B(4) birds than in their B(4)B(4) siblings.
In vitro susceptibility to thyroid hormone stimulation of membrane-associated Ca2+-ATPase activity has been examined in red blood cells from rat, rabbit, dog, monkey, and man. Monkey and human red cell Ca2+-ATPase activities responded comparably to 10(-10)M T4 or T3. Basal and thyroid hormone-stimulated Ca2+-ATPase activity in rabbit erythrocytes was four-fold higher than in primate red cells. Rat and dog red cell Ca2+-ATPase did not respond to iodothyronines in vitro.
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