title: Autoimmune thyroid disease: new models of cell death in autoimmunity.
abstract: Autoimmunity to thyroid antigens leads to two distinct pathogenic processes with opposing clinical outcomes: hypothyroidism in Hashimoto's thyroiditis and hyperthyroidism in Graves' disease. The high frequency of these diseases and easy accessibility of the thyroid gland has allowed the identification of key pathogenic mechanisms in organ-specific autoimmune diseases. In early investigations, antibody- and T-cell-mediated death mechanisms were proposed as being responsible for autoimmune thyrocyte depletion. Later, studies on apoptosis have provided new insights into autoimmune target destruction, indicating the involvement of death receptors and cytokine-regulated apoptotic pathways in the pathogenesis of thyroid autoimmunity.
authors.affiliation: Department of Surgical and Oncological Sciences, University of Palermo, Palermo, Italy.
authors.forename: Giorgio
authors.initials: G
authors.lastname: Stassi
authors.forename: Ruggero
authors.initials: R
authors.lastname: De Maria
mesh_terms: D017209:Apoptosis; D015551:Autoimmunity; D053222:Fas Ligand Protein; D006111:Graves Disease / Q000473:pathology*; D006801:Humans; D008562:Membrane Glycoproteins / Q000032:analysis; D023421:Models, Animal; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D013961:Thyroid Gland / Q000276:immunology / Q000473:pathology*; D013967:Thyroiditis, Autoimmune / Q000473:pathology*; D019014:fas Receptor / Q000032:analysis
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019014:fas Receptor