Cellular immunity in autoimmune thyroid disease.

Abstract

Autoimmune thyroid disease occurs in a genetically susceptible patient after triggering events including bacterial and viral infections, environmental insults, drugs or hormones. These triggering events may break the tolerance 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 this, 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 also 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 tissue-non-specific antigens. These immune responses may contribute to the recurring immunologic activity and maintenance of autoantibody overproduction.