Apoptosis and the thyroid: the Fas/Fas L pathway

Citation
V. Vlaeminck-guillem et al., Apoptosis and the thyroid: the Fas/Fas L pathway, PRESSE MED, 30(2), 2001, pp. 74-80
Citations number
57
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
PRESSE MEDICALE
ISSN journal
07554982 → ACNP
Volume
30
Issue
2
Year of publication
2001
Pages
74 - 80
Database
ISI
SICI code
0755-4982(20010120)30:2<74:AATTTF>2.0.ZU;2-9
Abstract
The apoptotic Fas/Fas-L pathway represents a major apoptotic pathway and in volves the specific interaction between a membrane receptor, Fas, harbored by the target cell and a membrane ligand, Fas-L, harbored by the cytotoxic cell. Fas and normal thyroid gland: Normal thyrocytes express Fas receptor but no t its ligand. The control of thyroid gland volume results from an equilibri um between the trophic action of TSH and thyrocyte apoptosis, which is limi ted to some extent by resistance to Fas activation by producing an inhibito r of the apoptotic signal transduction. Fas and Hashimoto's thyroiditis: Aberrant expression of Fas-L by thyrocytes induces their fratricide apoptosis. Thyroid-infiltrating lymphocytes are r esistant to apoptosis by overexpressing the antiapoptotic protein Bcl2. Fas and Graves' disease: Autoantibody-dependant stimulation of the thyrotro pin receptor favors goiter formation by reducing thyrocyte apoptosis. It in duces repression of Fas expression and production of a soluble Fas, whose s erum levels are correlated with clinical course. Fas and thyroid cancer: Tumoral cells are resistant to apoptosis by inhibit ing the apoptotic signal transduction and exert Fas counter-attack by induc ing apoptosis of antitumoral lymphocytes.