While the preceding construction cannot yet be supported in each detail by direct observations, it may be of value in helping to direct future studies on the pathogenesis of thyroid autoimmunity. It stresses the normal occurrence of immune self-reactivity, the genetic and environmental forces that may amplify such responses, the role of the antigen-driven immune attack, secondary disease-enhancing factors, and the important contributory role of antigen-independent immune reactivity. Least understood is the last area, that of clonal expansion involved in development of the associate immunological syndromes. Research on thyroid autoimmunity has benefited greatly by knowledge of the specific target antigens and easy access to blood cells and involved target tissue. As research moves now into the realm of molecular immunology and genetics, we may look for rapid progress in understanding and controlling these common illnesses.