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.
| Original language | English |
|---|---|
| Pages (from-to) | 19-23 |
| Number of pages | 5 |
| Journal | Journal of Clinical Immunology |
| Volume | 21 |
| DOIs | |
| Publication status | Published - 2001 |
Keywords
- CD95/APO-1
- apoptosis
- death receptors
- thyroid autoimmunity
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