title: Fas-FasL in Hashimoto's thyroiditis.
abstract: Hashimoto's thyroiditis is a common chronic autoimmune disease characterized by the loss of thyroid follicular cells (thyrocytes) that are gradually replaced by lymphocytic infiltration and diffuse fibrosis. These morphological findings suggested that autoreactive T-cell clones were responsible for thyrocyte destruction and hypothyroidism through effector-target cytotoxic recognition. Later, autonomous interaction between thyrocyte Fas and FasL has been proposed as a major mechanism of thyrocyte depletion in Hashimoto's thyroiditis. Here, we analyze the possible role of Fas and FasL in the pathogenesis of Hashimoto's thyroiditis. We suggest that the Fas-FasL system dictates the outcome of the autoimmune response by acting on both immune and target cells.
authors.affiliation: Department of Surgical, Anatomical and Oncological Sciences, University of Palermo, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Stassi
authors.forename: A
authors.initials: A
authors.lastname: Zeuner
authors.forename: D
authors.initials: D
authors.lastname: Di Liberto
authors.forename: M
authors.initials: M
authors.lastname: Todaro
authors.forename: L
authors.initials: L
authors.lastname: Ricci-Vitiani
authors.forename: R
authors.initials: R
authors.lastname: De Maria
mesh_terms: D017209:Apoptosis; D053222:Fas Ligand Protein; D006801:Humans; D008562:Membrane Glycoproteins / Q000502:physiology*; D013967:Thyroiditis, Autoimmune / Q000209:etiology*; D019014:fas Receptor / Q000502:physiology*
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019014:fas Receptor