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.