Thyroid cell apoptosis - A new understanding of thyroid autoimmunity

Citation
E. Phelps et al., Thyroid cell apoptosis - A new understanding of thyroid autoimmunity, END METAB C, 29(2), 2000, pp. 375
Citations number
115
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA
ISSN journal
08898529 → ACNP
Volume
29
Issue
2
Year of publication
2000
Database
ISI
SICI code
0889-8529(200006)29:2<375:TCA-AN>2.0.ZU;2-4
Abstract
Apoptosis is a highly regulated mechanism of cell death involved in normal development, immune regulation, and homeostasis. Abnormal apoptotic activit y has been implicated in a variety of diseases including cancer, autoimmuni ty, and degenerative disorders. In the thyroid, altered cell death may play a role in the pathogenesis of autoimmune disorders such as Hashimoto's thy roiditis and Graves' disease. Apoptosis-signaling pathways can be initiated through activation of death receptors or in response to cellular damage, s uch as in gamma irradiation. It has been demonstrated that Fas, tumor necro sis factor, and tumor necrosis factor-related apoptosis-inducing ligand pat hways are present and functional in the thyroid, although the expression of these molecules and their roles in thyroid autoimmunity have been debated. Thyroid apoptosis is regulated at multiple levels, including receptor and ligand expression, and the expression of anti-apoptotic proteins, such as F AP-1 and Bcl-2. These factors may provide potential mechanisms for modifyin g the pathogenesis of autoimmune thyroid disease.