Potential involvement of fas and its ligand in the pathogenesis of Hashimoto's thyroiditis

Carla Giordano, Giorgio Stassi, Ruggero De Maria, Matilde Todaro, Pierina Richiusa, Giuliana Papoff, Giovina Ruberti, Marcello Bagnasco, Roberto Testi, Aldo Galluzzo

Research output: Contribution to journalArticlepeer-review

Abstract

The mechanisms responsible for thyrocyte destruction in Hashimoto's thyroiditis (HT) are poorly understood. Thyrocytes from HT glands, but not from nonautoimmune thyroids, expressed Fas. Interleukin-1β (IL-1β), abundantly produced in HT glands, induced Fas expression in normal thyrocytes, and cross-linking of Fas resulted in massive thyrocyte apoptosis. The ligand for Fas (FasL) was shown to be constitutively expressed both in normal and HT thyrocytes and was able to kill Fas-sensitive targets. Exposure to IL-1β induced thyrocyte apoptosis, which was prevented by antibodies that block Fas, suggesting that IL-1β-induced Fas expression serves as a limiting factor for thyrocyte destruction. Thus, Fas-FasL interactions among HT thyrocytes may contribute to clinical hypothyroidism.

Original languageEnglish
Pages (from-to)960-963
Number of pages4
JournalScience
Volume275
Issue number5302
Publication statusPublished - Feb 14 1997

ASJC Scopus subject areas

  • General

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