AUTOIMMUNE THYROID-DISEASE - IMMUNOLOGICAL MODEL AND CLINICAL PROBLEM

Thyroid autoimmunity can be regarded as the prototype of organ-specifi c autoimmune disease. Manifestations of human thyroid autoimmunity inc lude thyroid hyper- or hypofunction and thyroid enlargment or atrophy, resulting. in different clinical diseases. Only few autoantigens are clearly characterized. Several genetic or environmental factors are hy pothesized to play a predisposing or triggering role. A crucial point in the development of thyroid autoimmunity is the localization within the thyroid of immunocompetent cells able to clonally proliferate in r esponse to autoantigens, to promote recruitment of additional infiltra ting cells, and eventually to drive different B and T cell-mediated im munopathological reactions. In this context it is important to analyze the functional repertoire of intrathyroid T cells, in addition to the ir specificities, and the possible differences between Graves' disease and Hashimoto's thyroiditis. The ability of lymphoid cells to localiz e within the tissue, and the nature of their interaction with follicul ar thyroid cells is determined by the expression of adhesion molecules . The presence of different adhesion molecules (in addition to MHC ant igens) on thyroid epithelial cells is a critical phenomenon, in the li ght of their hypothesized, although controversal, ability to present a utoantigenic peptides. Such a phenomenon is even more important for th yroid epithelial cell targeting by cytotoxic effector cells. Differenc es between Graves' disease and Hashimoto's thyroiditis have been obser ved, consistently with an important role of cytotoxicity in the latter disease. Finally, treatment of human autoimmune thyroid disease is ma inly directed to correct thyroid hyper- or hypofunction; however it ma y probably also affect the course of the autoimmune process (Fund. Cli n. Immunol. 4: 7-27, 1996).