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Editorial
APOPTOSIS IN AUTOIMMUNE AND NON-AUTOIMMUNE THYROID DISEASE
Article first published online: 19 APR 1999
DOI: 10.1002/(SICI)1096-9896(199706)182:2<123::AID-PATH832>3.0.CO;2-F
Copyright © 1997 John Wiley & Sons, Ltd.
1096-9896/asset/cover.gif?v=1&s=9d27ae473c5444468836a93370dc054fd0ea594f "The Journal of Pathology")
Additional Information
How to Cite
LUDGATE, M. and JASANI, B. (1997), APOPTOSIS IN AUTOIMMUNE AND NON-AUTOIMMUNE THYROID DISEASE. J. Pathol., 182: 123–124. doi: 10.1002/(SICI)1096-9896(199706)182:2<123::AID-PATH832>3.0.CO;2-F
Publication History
- Issue published online: 19 APR 1999
- Article first published online: 19 APR 1999
- Manuscript Accepted: 13 DEC 1996
- Manuscript Received: 5 DEC 1996
- Abstract
- References
- Cited By
Keywords:
- apoptosis;
- autoimmune thyroid disease;
- FAS;
- FAS-L;
- cytotoxic T cell
Abstract
The elimination of autoreactive T cells in the thymus involves the process of programmed cell death. Animal model studies, using the lpr and gld strains of mice, have identified FAS receptor (FAS) and FAS ligand (FAS-L) as important components of this mechanism. Whether FAS and FAS-L are also implicated in the autoimmune destruction of a target organ, 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 culture and in intact thyroid tissues obtained from Hashimoto's thyroiditis, multinodular 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. © 1997 John Wiley & Sons, Ltd.