Autoimmune endocrinopathies.

Abstract

A great deal of understanding of the human autoimmune endocrinopathies has come from studies of thyroiditis in experimental animals. Three such models are available: induced thyroiditis produced by injections of thyroglobulin plus adjuvant; spontaneous thyroiditis in genetically susceptible animals; and thyroiditis resulting from manipulation of the immunological apparatus. The major lessons learned from studies of experimental animals are (i) autoimmune disease is multifactorial and polygenic; (ii) one or more genes regulating the immune response are associated with the major histocompatibility complex (Mhc) of the particular species; (iii) genetic control of tissue damage is more restricted than control of autoantibody formation; (iv) the Mhc controls T-cell proliferation to the autoantigens; (v) a distinct population of T cells prevents the development of organ-specific autoimune disease; (vi) the suppressor population emigrates from the thymus at a time and rate different from the helper populations; (vii) the suppressor population is more susceptible to low levels of irradiation and to cytotoxic effects of antiserum to Lyt-1 than is the helper population.