APOPTOSIS IN AUTOIMMUNE AND NON-AUTOIMMUNE THYROID-DISEASE

Citation
M. Ludgate et B. Jasani, APOPTOSIS IN AUTOIMMUNE AND NON-AUTOIMMUNE THYROID-DISEASE, Journal of pathology, 182(2), 1997, pp. 123-124
Citations number
13
Categorie Soggetti
Pathology
Journal title
ISSN journal
00223417
Volume
182
Issue
2
Year of publication
1997
Pages
123 - 124
Database
ISI
SICI code
0022-3417(1997)182:2<123:AIAANT>2.0.ZU;2-J
Abstract
The elimination of autoreactive T cells in the thymus involves the pro cess of programmed cell death. Animal model studies, using the Ipi and gld strains of mice, have identified FAS receptor (FAS) and FAS ligan d (FAS-L) as important components of this mechanism. Whether FAS and F AS-L are also implicated in the autoimmune destruction of a target org an, such as the thyroid, remain hypothetical. An accompanying paper in this issue has addressed the question by FACS and immunocytochemical analysis of FAS expression and apoptosis in thyrocytes grown in cultur e and in intact thyroid tissues obtained from Hashimoto's thyroiditis, multimodular goitre and Graves' disease. The overall results suggest that the degree of FAS expression on target cells may determine their sensitivity to T-cell mediated cytotoxicity in the absence of perforin or granzyme directed apoptosis mechanisms. (C) 1997 by John Wiley & S ons, Ltd.