Fas-FasL in Hashimoto's thyroiditis

被引:29
作者
Stassi, G
Zeuner, A
Di Liberto, D
Todaro, M
Ricci-Vitiani, L
De Maria, R
机构
[1] Ist Super Sanita, Lab Hematol & Oncol, I-00161 Rome, Italy
[2] Univ Palermo, Human Anat Sect, Dept Surg Anat & Oncol Sci, I-90127 Palermo, Italy
[3] Univ Catania, Inst Gen Pathol, I-95124 Catania, Italy
关键词
thyroid autoimmunity; apoptosis; death receptors; CD95/APO-1;
D O I
10.1023/A:1006732713634
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:19 / 23
页数:5
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