Structure-function relationships in the mechanisms by which glycoprotein hormones (thyrotropin), autoantibodies, certain bacterial toxins (cholera and pertussis, for example), the anti- viral protective agent, interferon, alpha1-adrenergic agents, insulin, and insulin-like growth factors (I and II) interact with and transmit their message through the cell membrane to affect thyroid or fibroblast function and pathology are being defined. Studies using monoclonal antibodies and the idiotype antiidiotype theory have continued to explore the importance of these relationships to the expression of thyroid hyperfunction in Graves' disease; to organ-specific autoimmunity in general, and the auto immunity of Graves' disease, Hashimoto's disease, and diabetes in particular; to fluid losses in intestinal diarrhetic states; to thyroid storm and the sympathetic overactivity syndrome of tetanus; to the ability of hormones to modulate the oncogenic state; and to the mechanism by which toxins subvert normal mechanisms to impose their pathological effects. Studies have been continued which evaluate the role of different hormones and signal transduction mechanisms in thyroglobulin biosynthesis, in thyroglobulin biodegradation to T3 and T4, and in the transport of T3, T4, moniodotyrosine, diiodotyrosine, and other amino acids from the lysosome. The role of phosphate and carbohydrate moieties in thyroglobulin structure and post-translational processing is being studied. Studies also continue to explore lipid regulation of receptor expression with special emphasis on neuronal and thyroid cell growth and development. Studies have been initiated to clone the TSH receptor and define its structure and regulatory control at a gene level.