Abstract
Autoimmune thyroid disease occurs in a genetically susceptible patients after triggering events including bacterial and viral infections, environmental insults, drugs or hormones. These triggering events may break the tolerance or anergy to self antigen, leading to emergence of autoreactive T cells. One or more T cell clones that recognize the self antigen is (are) assumed to be involved in initiating autoimmune processes. Following thus, T cell clones expand and migrate from the peripheral blood into the thyroid gland. Migration of mononuclear cells is controlled by inflammatory cytokines and adhesion molecules.
Intrathyroidal T cells may interact with dendritic-like cells, thyrocytes expressed with HLA-DR antigens, B cells and extracellular matrix, resulting in the proliferation of T cells, production of cytokines and autoantibodies. These interactions are regulated by inflammatory cytokines and adhesion molecules. When the initial immune response is completed, a secondary immune response ensues, that may be of considerable complexity involving reaction of infiltrating T cells to a variety of tissue-specific and tissuenonspecific antigens.
These immune responses may contribute to the recurring immunologic activity and maintenance of autoantibody overproduction.
