| Literature DB >> 11321234 |
G Stassi1, A Zeuner, D Di Liberto, M Todaro, L Ricci-Vitiani, R De Maria.
Abstract
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.Entities:
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Year: 2001 PMID: 11321234 DOI: 10.1023/a:1006732713634
Source DB: PubMed Journal: J Clin Immunol ISSN: 0271-9142 Impact factor: 8.317