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Trends Endocrinol Metab. 2001 Nov;12(9):384-90.

Apoptosis induced by FasL and TRAIL/Apo2L in the pathogenesis of thyroid diseases.

Author information

1
Department of Adult Oncology, Dana-Farber Cancer Institute, Mayer Building, Room M557, 44 Binney Street, Boston, MA 02115, USA. mitsiades@netscape.net

Abstract

FasL and TRAIL/Apo2L participate in cell-mediated cytotoxicity by inducing apoptosis in susceptible cells via respective cell surface receptors. Normal and neoplastic thyroid tissues are resistant to FasL-induced apoptosis but are sensitized by Th-1-type cytokines. In Hashimoto's thyroiditis, both FasL and its receptor, Fas, are strongly upregulated and their interaction leads to the suicidal/fratricidal death of thyrocytes. In Graves' disease, FasL expression in thyroid follicular cells is induced by thionamides and kills infiltrating lymphocytes. In this condition, Th-2-type cytokines upregulate the anti-apoptotic molecules FLIP and Bcl-x(L) and protect thyrocytes from apoptosis. FasL is expressed by neoplastic thyrocytes and induces apoptosis of infiltrating lymphocytes. TRAIL/Apo2L kills thyroid carcinoma cells but spares normal thyrocytes, thus providing a potential therapy for thyroid cancer.

PMID:
11595539
[Indexed for MEDLINE]

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