The role of Fas-mediated apoptosis in thyroid disease

被引:38
作者
Andrikoula, M [1 ]
Tsatsoulis, A [1 ]
机构
[1] Univ Ioannina, Sch Med, Dept Med, Div Endocrinol, GR-45110 Ioannina, Greece
关键词
D O I
10.1530/eje.0.1440561
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Recent evidence has emphasized the importance of apoptosis in the maintenance of tissue homeostasis and the pathogenesis of malignant and immune diseases. Autoimmune thyroid diseases such as Hashimoto's thyroiditis and Graves' disease, as well as other autoimmune endocrine diseases, have been associated with dysregulation of apoptotic signaling pathways. In particular, dysfunction of the Fas apoptotic pathway or production of soluble factors including soluble Fas and soluble Fas ligand may be involved in the pathogenesis of these disorders. On the other hand, malignant thyroid cells may avoid Fas-mediated suicide possibly by expression of inhibitors of apoptosis and evade the immune system by inducing apoptosis on infiltrating lymphocytes. The delicate balance between cell proliferation and cell death through the Fas pathway may also play an important role in the control of thyroid cell mass and goitrogenesis. This review analyzes the current evidence on the role of Fas-mediated apoptosis in the pathogenesis of thyroid diseases including Hashimoto's thyroiditis, Graves' disease, thyroid cancer and goiter. However, the exact mechanisms involved in the regulation of apoptosis in thyroid disease remain unclear. Further investigation is needed.
引用
收藏
页码:561 / 568
页数:8
相关论文
共 52 条
[1]   The origin of programmed cell death [J].
Ameisen, JC .
SCIENCE, 1996, 272 (5266) :1278-1279
[2]   Apoptosis and thyroiditis [J].
Arscott, PL ;
Baker, JR .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1998, 87 (03) :207-217
[3]   Fas (APO-1, CD95)-mediated apoptosis in thyroid cells is regulated by a labile protein inhibitor [J].
Arscott, PL ;
Knapp, J ;
Rymaszewski, M ;
Bartron, JL ;
Bretz, JD ;
Thompson, NW ;
Baker, JR .
ENDOCRINOLOGY, 1997, 138 (11) :5019-5027
[4]   Death receptors: Signaling and modulation [J].
Ashkenazi, A ;
Dixit, VM .
SCIENCE, 1998, 281 (5381) :1305-1308
[5]   Forging a path to cell death [J].
Barinaga, M .
SCIENCE, 1996, 273 (5276) :735-737
[6]   A ROLE FOR CD95 LIGAND IN PREVENTING GRAFT-REJECTION [J].
BELLGRAU, D ;
GOLD, D ;
SELAWRY, H ;
MOORE, J ;
FRANZUSOFF, A ;
DUKE, RC .
NATURE, 1995, 377 (6550) :630-632
[7]   DIFFERENTIAL AUTOANTIBODY RESPONSES TO THYROID PEROXIDASE IN PATIENTS WITH GRAVES-DISEASE AND HASHIMOTO THYROIDITIS [J].
BERMANN, M ;
MAGEE, M ;
KOENIG, RJ ;
KAPLAN, MM ;
ARSCOTT, P ;
MAASTRICHT, J ;
JOHNSON, J ;
BAKER, JR .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1993, 77 (04) :1098-1101
[8]   Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death [J].
Boldin, MP ;
Goncharov, TM ;
Goltsev, YV ;
Wallach, D .
CELL, 1996, 85 (06) :803-815
[9]   PROTECTION FROM FAS-MEDIATED APOPTOSIS BY A SOLUBLE FORM OF THE FAS MOLECULE [J].
CHENG, JH ;
ZHOU, T ;
LIU, CD ;
SHAPIRO, JP ;
BRAUER, MJ ;
KIEFER, MC ;
BARR, PJ ;
MOUNTZ, JD .
SCIENCE, 1994, 263 (5154) :1759-1762
[10]   The role of Fas in autoimmune diabetes [J].
Chervonsky, AV ;
Wang, Y ;
Wong, FS ;
Visintin, I ;
Flavell, RA ;
Janeway, CA ;
Matis, LA .
CELL, 1997, 89 (01) :17-24