Fas-FasL in Hashimoto's thyroiditis

Ruggero De Maria Marchiano, Giorgio Stassi, Ann Zeuner, Diana Di Liberto, Matilde Todaro, Lucia Ricci-Vitiani

Research output: Contribution to journalArticle

31 Citations (Scopus)


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
Publication statusPublished - 2001


  • CD95/APO-1
  • apoptosis
  • death receptors
  • thyroid autoimmunity


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