Selective IgA deficiency in chickens with spontaneous autoimmune thyroiditis.

Abstract

SELECTIVE IgA deficiency is believed to be the commonest form of human immunodeficiency disease, and occurs with a frequency of between 1: 500 and 1: 700 in random populations1,2. Although the isolated deficiency is often considered non-pathological, there is clinical and laboratory evidence that IgA-deficient individuals suffer more sinopulmonary infection and autoimmune and gastrointestinal disorders3,4. Family studies have suggested a genetic factor but no defined inheritance patterns have been established4,5. The chicken model has been used for a number of years in our laboratory to study the ontogeny of immunoglobulin class development6. Surgical bursectomy at hatching7,8, treatment of chick embryos with specific antisera7,9–11 and combined neonatal bursectomy–thymectomy12 can result in depressed levels of IgA. This report describes recent observations of a selective IgA-deficiency that spontaneously occurs in the Obese strain (OS) of White Leghorn chickens. The OS chickens develop spontaneous autoimmune thyroiditis (SAT) at several weeks of age13. Clinical hypothyroidism is observed and high litres of circulating as well as bound anti-thyroglobulin antibodies can be detected14. The OS chickens were initially derived from the Cornell C-strain which reveals a 1% incidence of SAT. Selective breeding of CS birds, which showed phenotypic symptoms of hypothyroidism, resulted in the OS of which now, in generations 16 and 17, show 96% SAT. The histolegical and serological features in OS chickens make it a reasonable animal model to study Hashimoto's thyroiditis, an autoimmune disorder in humans15.