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J Biol Chem, Vol. 274, Issue 36, 25433-25438, September 3, 1999
From the Department of Medicine, University of Michigan Medical
Center, Ann Arbor, Michigan, 48109-0648
The occurrence of apoptosis in thyroid follicular
cells induced by Fas activation has been a subject of much debate. This is due, in part, to the fact that no physiologically relevant treatment
conditions have been reported to cause rapid and extensive Fas-mediated
apoptosis in thyroid cells, whereas treatment with the protein
synthesis inhibitor cycloheximide prior to Fas activation allows for
massive cell death. This indicates that the Fas signaling pathway is
present but that its function is blocked in the overwhelming majority
of cultured thyroid cells. To reconcile the conflicting reports, we set
out to identify physiologically relevant conditions in which rapid,
massive thyroid cell apoptosis in response to Fas activation could be
demonstrated. We determined that susceptibility to Fas-activated
apoptosis could be influenced by certain combinations of
inflammatory cytokines. Although no single cytokine was effective, pretreatment of thyroid cells with the combination of 
-interferon and either tumor necrosis factor-
or interleukin 1
allowed for massive Fas-mediated apoptosis. Susceptibility to Fas-induced death
correlated with an increase in expression of a tunicamycin-inhibitable high molecular weight form of Fas but not with aggregate expression of Fas.
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