The Obese Strain of Chickens: An Animal Model with Spontaneous Autoimmune Thyroiditis

Thyroid glands of Obese Strain (OS) chickens become severely infiltrated by mononuclear cells and the occurrence of numerous germinal centers is a characteristic histological hallmark of the disease. Autoimmune thyroid destruction leads to thyroid hormone deficiency that entails the development of hypothyroid symptoms, such as small body size; massive subcutaneous and abdominal fat deposits (hence the name); lipid serum; long, silky feathers; small combs; cold sensitivity; low fertility; and poor hatching ability. The serum of 0s chickens contains AAbs to Tg, microsomal antigens, and T3 and T4. Tg-AAb formation is not because of polyclonal activation, but requires the presence of the autoantigen. The infiltrated thyroid itself has been identified as the major Tg-AAb-producing organ and can be the site of the formation of antibodies against exogenous antigens. OS chickens also produce AAbs against a variety of other organ-specific and non-organ-specific antigens, albeit with significantly lower frequency and titers, and without concomitant histopathological or functional lesions, such as Addison-like disease or diabetes mellitus. Additionally, factors extrinsic to the immune system that also affect immunoregulation have been found to be altered in the OS. Thus, OS chickens display a significantly decreased glucocorticoid tonus because of an increased serum concentration of corticosteroid-binding globulin and therefore markedly decreased free, metabolically active glucocorticoids.