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Cited by 582

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Potential Involvement of Fas and Its Ligand in the Pathogenesis of Hashimoto's Thyroiditis

Giordano, Carla, Stassi, Giorgio, De Maria, Ruggero, Todaro, Matilde, Richiusa, Pierina, Papoff, Giuliana, Ruberti, Giovina, Bagnasco, Marcello, Testi, Roberto, Galluzzo, Aldo·1997·Science

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.

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Metadata

Authors
Giordano, C., Stassi, G., De Maria, R., Todaro, M., Richiusa, P., Papoff, G., Ruberti, G., Bagnasco, M., Testi, R., & Galluzzo, A.
Venue
Science
Published
1997-02-14
Volume
275
Issue
5302
Pages
960-963
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W1514099677
Cited by
582
References
1
FWCI
56.83
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Potential Involvement of Fas and Its Ligand in the Pathogenesis of Hashimoto's Thyroiditis. https://app.cochat.ai/papers/10.1126/science.275.5302.960
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Giordano, C., Stassi, G., De Maria, R., Todaro, M., Richiusa, P., Papoff, G., Ruberti, G., Bagnasco, M., Testi, R., & Galluzzo, A. (1997). Potential Involvement of Fas and Its Ligand in the Pathogenesis of Hashimoto's Thyroiditis. Science. https://doi.org/10.1126/science.275.5302.960

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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