Fas-FasL in Hashimoto's thyroiditis

G. Stassi, A. Zeuner, D. Di Liberto, M. Todaro, L. Ricci-Vitiani, R. De Maria

Research output: Contribution to journalArticlepeer-review


Hashimoto's thyroiditis is a common chronic autoimmune disease characterized by the loss of thyroid follicular cells (thyrocytes) that are gradually replaced by lymphocytic infiltration and diffuse fibrosis. These morphological findings suggested that autoreactive T-cell clones were responsible for thyrocyte destruction and hypothyroidism through effector-target cytotoxic recognition. Later, autonomous interaction between thyrocyte Fas and FasL has been proposed as a major mechanism of thyrocyte depletion in Hashimoto's thyroiditis. Here, we analyze the possible role of Fas and FasL in the pathogenesis of Hashimoto's thyroiditis. We suggest that the Fas-FasL system dictates the outcome of the autoimmune response by acting on both immune and target cells.

Original languageEnglish
Pages (from-to)19-23
Number of pages5
JournalJournal of Clinical Immunology
Issue number1
Publication statusPublished - 2001


  • Apoptosis
  • CD95/APO-1
  • Death receptor
  • Thyroid autoimmunity

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy


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