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.