The role of Fas-mediated apoptosis in thyroid autoimmune disease

Apoptosis is a carefully regulated mechanism of cell death that differs fro m necrosis and plays an important role in normal tissue development and hom eostasis, as well as disease processes, Apoptosis also plays an important r ole in autoimmunity. Defective apoptosis can cause systemic autoimmunity by allowing the survival of autoreactive lymphocytes. It may also be involved in the pathogenesis of organ-specific autoimmune diseases, such as Hashimo to's thyroiditis, through altered target organ susceptibility. Apoptosis si gnaling pathways can be initiated through activation of death receptors. On e of these pathways employs the death receptor Fas and its ligand (FasL). F as expression and death pathway signaling have been demonstrated in the thy roid, but there is controversy surrounding the expression of FasL and its r ole in thyroid autoimmunity. A number of proteins, including FAP-1, Bcl-2 a nd I-FLICE may regulate the Fas pathway in the thyroid and provide potentia l mechanisms for modifying the pathogenesis of autoimmune thyroid disease.