Inflammatory cytokine regulation of TRAIL-mediated apoptosis in thyroid epithelial cells

J. D. Bretz, E. Mezosi, T. J. Giordano, P. G. Gauger, N. W. Thompson, J. R. Baker

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

Death receptor-mediated apoptosis has been implicated in target organ destruction in chronic autoimmune thyroiditis. Depending on the circumstances, inflammatory cytokines such as IL-1, TNF and IFNγ have been shown to contribute to either the induction, progression or inhibition of this disease. Here we demonstrate that the death ligand TRAIL can induce apoptosis in primary, normal, thyroid epithelial cells under physiologically relevant conditions, specifically, treatment with the combination of inflammatory cytokines IL-1β and TNFα. In contrast, IFNγ is capable of blocking TRAIL-induced apoptosis in these cells. This regulation of TRAIL-mediated apoptosis by inflammatory cytokines appears to be due to alterations of cell surface expression of TRAIL receptor DR5 and not DR4. We also show the in vivo presence of TRAIL and TRAIL receptors DR5 and DcR1 in both normal and inflamed thyroids. Our data suggests TRAIL-mediated apoptosis may contribute to target organ destruction in chronic autoimmune thyroiditis.

Original languageEnglish
Pages (from-to)274-286
Number of pages13
JournalCell Death and Differentiation
Volume9
Issue number3
DOIs
Publication statusPublished - Mar 25 2002

Keywords

  • Apoptosis
  • Autoimmune disease
  • Death receptor 5
  • Decoy receptor
  • Inflammatory cytokine
  • Interferon gamma

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'Inflammatory cytokine regulation of TRAIL-mediated apoptosis in thyroid epithelial cells'. Together they form a unique fingerprint.

  • Cite this