The immunological basis of autoimmune disease.

Organ-specific diseases often involve cell surface antigens which when functionally characterized prove to have some receptor function. Certain restricted parts of the molecule are autoantigenic but the response to these epitopes is similar to that provoked by foreign antigens with respect to diversity of class, clonality and probably idiotypy. The mechanisms controlling the response to components on the surface of the body's cells are not fully understood but might be circumvented by polyclonal activators or by the development of T suppressor dysfunction. The latter could occur through a generalized defect in T suppressor cells, which would account for the association of autoimmune diseases in given individual subjects. Alternatively, or in addition (since genetic studies suggest multifactorial influences), the suppressor defect could be antigen specific. Our studies in chickens with spontaneous autoimmune thyroiditis show that normal antigen is obligatory for both the development and maintenance of autoantibody production and that it is possible that some abnormality or change in the presentation of the autoantigen (rather than its structure) is concerned in the initiation process.