APOPTOSIS AND THYROIDITIS

Citation
Pl. Arscott et Jr. Baker, APOPTOSIS AND THYROIDITIS, Clinical immunology and immunopathology (Print), 87(3), 1998, pp. 207-217
Citations number
100
Categorie Soggetti
Pathology,Immunology
ISSN journal
00901229
Volume
87
Issue
3
Year of publication
1998
Pages
207 - 217
Database
ISI
SICI code
0090-1229(1998)87:3<207:>2.0.ZU;2-6
Abstract
The origin of the various forms of autoimmune thyroiditis remains uncl ear. Most investigations into the pathogenesis of these disorders have focused on immune abnormalities that might lead to an autoimmune resp onse. However, no unique immune response to thyroid autoantigens has b een identified that either is limited to patients with thyroiditis or is absolutely correlated with clinical disease expression. CD8 T-cell- mediated cytotoxicity is thought to be a major cause of thyroid follic ular cell damage in thyroiditis. This damage is produced in part throu gh the induction of apoptosis in thyroid cells. Recent studies have de monstrated that programmed cell death is regulated in thyroid cells an d that a major pathway for immune-mediated apoptosis, the Fas pathway, is blocked by labile inhibitors in a manner that could prevent cytoto xicity. This review also examines several other types of regulation of apoptotic pathways in thyrocytes. We hypothesize that the regulation of programmed cell death pathways in the thyroid may alter the express ion of autoimmune thyroid diseases by modifying the susceptibility of thyroid cells to immune-mediated apoptosis. (C) 1998 Academic Press.