Fas/Fas ligand up-regulation and Bcl-2 down-regulation may be significant in the pathogenesis of Hashimoto's thyroiditis.
Title | Fas/Fas ligand up-regulation and Bcl-2 down-regulation may be significant in the pathogenesis of Hashimoto's thyroiditis. |
Publication Type | Journal Article |
Year of Publication | 1998 |
Authors | Mitsiades, N., Poulaki V., Kotoula V., Mastorakos G., Tseleni-Balafouta S., Koutras D. A., & Tsokos M. |
Journal | J Clin Endocrinol Metab |
Volume | 83 |
Issue | 6 |
Pagination | 2199-203 |
Date Published | 1998 Jun |
ISSN | 0021-972X |
Keywords | Adolescent, Adult, Apoptosis, Cross-Linking Reagents, Fas Ligand Protein, fas Receptor, Female, Humans, Male, Membrane Glycoproteins, Middle Aged, Proto-Oncogene Proteins c-bcl-2, Thyroid Gland, Thyroiditis, Autoimmune |
Abstract | Hashimoto's thyroiditis (HT) is an autoimmune disorder characterized by diffuse thyroid lymphocytic infiltration and follicle destruction. Cross-linking of the Fas receptor with its own ligand (FasL) triggers apoptosis in various systems, whereas the Bcl-2 protooncogene inhibits apoptotic cell death. The involvement of Fas, FasL, and Bcl-2 in the apoptotic process in HT was evaluated in 15 thyroid tissue samples from patients with HT stained for apoptosis and for Fas, FasL, and Bcl-2 protein expression. Eight samples from healthy thyroid tissue were used for comparison. Thyroid follicles in HT samples exhibited strong staining for Fas and FasL and a high percentage of apoptosis (30.3 +/- 14.5%, mean +/- SD), in contrast to normal control follicles that exhibited moderate Fas, minimal or no FasL, and hardly any apoptosis. Immunostaining for Bcl-2 was high in normal, and weak in involved, thyroid follicles. Infiltrating lymphocytes stained weakly for FasL and strongly for Bcl-2. We conclude that follicular cells in HT undergo apoptosis by concomitant up-regulation of FasL and Fas and down-regulation of Bcl-2 protein. The lymphocytes do not seem to be directly engaged in the process with their own FasL, but they may provide the appropriate cytokine milieu that, in turn, up-regulates Fas and/or FasL leading to apoptosis. |
DOI | 10.1210/jcem.83.6.4853 |
Alternate Journal | J Clin Endocrinol Metab |
PubMed ID | 9626160 |