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[Apoptosis in Hashimoto's thyroiditis]

T Kotani1, Y Aratake, S Ohtaki

  • 1Institute for Clinical Investigation, Miyazaki Medical College Hospital.

Rinsho Byori. the Japanese Journal of Clinical Pathology
|December 13, 1997
PubMed
Summary

FasL, constitutively expressed on thyroid cells, interacts with Fas, induced by IL-1 beta, to cause apoptosis in Hashimoto's thyroiditis. This mechanism explains follicular epithelial cell death in this autoimmune disease.

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Area of Science:

  • Immunology
  • Cell Biology
  • Endocrinology

Background:

  • Autoimmune diseases involve apoptosis.
  • Hashimoto's thyroiditis, an organ-specific autoimmune disease, shows follicular epithelial cell death.
  • Fas-FasL-mediated apoptosis is implicated in this cell death.

Purpose of the Study:

  • To investigate the role of Fas-FasL-mediated apoptosis in Hashimoto's thyroiditis pathogenesis.
  • To examine DNA fragmentation and expression of Fas and FasL in thyroid tissues.
  • To clarify the in vitro mechanisms of follicular epithelial cell apoptosis.

Main Methods:

  • TUNEL assay for DNA fragmentation in thyroid tissue.
  • Electron microscopy to support TUNEL findings.
  • Immunohistochemistry for Fas and FasL expression.
  • In vitro studies on follicular epithelial cells.

Main Results:

  • Increased DNA fragmentation in thyroid follicles near lymphoid aggregates in Hashimoto's thyroiditis.
  • Strong Fas and FasL expression on follicular epithelial cells in Hashimoto's thyroiditis and thyroid cancer, but not Graves' disease or goiter.
  • Constitutive FasL expression and IL-1 beta-induced Fas expression on epithelial cells, leading to apoptosis.

Conclusions:

  • Fas-FasL pathway is a key mechanism for follicular epithelial cell death in Hashimoto's thyroiditis.
  • IL-1 beta stimulation induces Fas expression, facilitating apoptosis.
  • The interaction between constitutively expressed FasL and induced Fas leads to epithelial cell death.

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