Differential expression of Fas system apoptotic molecules in peripheral lymphocytes from patients with Graves' disease and Hashimoto's thyroiditis

被引:22
作者
Fountoulakis, Stelios [1 ]
Vartholomatos, George [2 ]
Kolaitis, Nikolaos [2 ]
Frillingos, Stathis [3 ]
Philippou, George [1 ]
Tsatsoulis, Agathocles [1 ]
机构
[1] Univ Ioannina, Sch Med, Dept Endocrinol, GR-45110 Ioannina, Greece
[2] Univ Hosp Ioannina, Hematol Lab, Mol Biol Unit, Ioannina 45110, Greece
[3] Univ Ioannina, Sch Med, Biol Chem Lab, GR-45110 Ioannina, Greece
关键词
D O I
10.1530/EJE-08-0092
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: To examine whether the Fas system apoptotic molecules are differentially expressed in Graves' disease (GD) and Hashimoto's thyroiditis (HT), the two opposite phenotypes of autoimmune thyroid disease (AITD). Design: The expression of Fas and Fas ligand (FasL) on peripheral CD4 and CD8 lymphocytes. and non-lymphoid immune cells as well as their soluble forms in serum from untreated patients with GD and HT were evaluated. Methods: Flow cytometry was performed for the study of peripheral immune cells from 70 newly diagnosed patients with AITD (55 with HT and 15 with GD) and 20 controls. ELISA was used for the measurement of soluble Fas (sFas) in serum samples from a subgroup of 35 AITD patients. Results: An increase in the proportion of CD4 and CD8 cells expressing Fas was found in both GD and HT. albeit with some differences, when compared with controls. Importantly, in GD patients, the intensity of Fas expression on CD4 and CD8 lymphocytes was reduced and sFas levels in serum were simultaneously increased when compared with HT patients and controls. Conclusions: The Fas system apoptotic molecules appear to be differentially expressed on peripheral lymphocytes in the two opposite phenotypes of AITD.
引用
收藏
页码:853 / 859
页数:7
相关论文
共 36 条
  • [1] The role of Fas-mediated apoptosis in thyroid disease
    Andrikoula, M
    Tsatsoulis, A
    [J]. EUROPEAN JOURNAL OF ENDOCRINOLOGY, 2001, 144 (06) : 561 - 568
  • [2] Fas (APO-1, CD95)-mediated apoptosis in thyroid cells is regulated by a labile protein inhibitor
    Arscott, PL
    Knapp, J
    Rymaszewski, M
    Bartron, JL
    Bretz, JD
    Thompson, NW
    Baker, JR
    [J]. ENDOCRINOLOGY, 1997, 138 (11) : 5019 - 5027
  • [3] The role of Fas-mediated apoptosis in thyroid autoimmune disease
    Borgerson, KL
    Bretz, JD
    Baker, JR
    [J]. AUTOIMMUNITY, 1999, 30 (04) : 251 - 264
  • [4] Percutaneous vertebroplasty for the treatment of burst fractures - Case report
    Chen, JF
    Wu, CT
    Lee, ST
    [J]. JOURNAL OF NEUROSURGERY-SPINE, 2004, 1 (02) : 228 - 231
  • [5] PROTECTION FROM FAS-MEDIATED APOPTOSIS BY A SOLUBLE FORM OF THE FAS MOLECULE
    CHENG, JH
    ZHOU, T
    LIU, CD
    SHAPIRO, JP
    BRAUER, MJ
    KIEFER, MC
    BARR, PJ
    MOUNTZ, JD
    [J]. SCIENCE, 1994, 263 (5154) : 1759 - 1762
  • [6] Soluble Fas is increased in hyperthyroidism independent of the underlying thyroid disease
    Feldkamp, J
    Pascher, E
    Schott, M
    Goretzki, P
    Seissler, J
    Scherbaum, NA
    [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2001, 86 (09) : 4250 - 4253
  • [7] On the pathogenesis of autoimmune thyroid disease: a unifying hypothesis
    Fountoulakis, S
    Tsatsoulis, A
    [J]. CLINICAL ENDOCRINOLOGY, 2004, 60 (04) : 397 - 409
  • [8] Differential regulation of Fas-mediated apoptosis in both thyrocyte and lymphocyte cellular compartments correlates with opposite phenotypic manifestations of autoimmune thyroid disease
    Giordano, C
    Richiusa, P
    Bagnasco, M
    Pizzolanti, G
    Di Blasi, F
    Sbriglia, MS
    Mattina, A
    Pesce, G
    Montagna, P
    Capone, F
    Misiano, G
    Scorsone, A
    Pugliese, A
    Galluzzo, A
    [J]. THYROID, 2001, 11 (03) : 233 - 244
  • [9] Thyrocyte targets and effectors of autoimmunity: A role for death receptors?
    Hammond, LJ
    Palazzo, FF
    Shattock, M
    Goode, AW
    Mirakian, R
    [J]. THYROID, 2001, 11 (10) : 919 - 927
  • [10] Hammond LJ, 1997, J PATHOL, V182, P138, DOI 10.1002/(SICI)1096-9896(199706)182:2<138::AID-PATH810>3.0.CO