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Cycloheximide inhibits interferon-gamma-induced class II major histocompatibility complex antigen expression in

M S Lee1, B Y Cho, S Y Kim

  • 1Department of Internal Medicine, Korea Cancer Center Hospital, Seoul.

Endocrinology
|March 1, 1991
PubMed

Insights

Interferon-gamma (IFN gamma) induces rat class II major histocompatibility complex antigen (RT1.B) expression in thyroid cells. This process requires new protein synthesis and is independent of calcium signaling pathways.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Class II Major Histocompatibility Complex (MHC) antigens are crucial for immune responses.
  • Interferon-gamma (IFN gamma) is a key cytokine involved in immune regulation.
  • Thyroid cells express MHC antigens under specific conditions.

Purpose of the Study:

  • To investigate the intracellular mechanisms by which IFN gamma induces Class II MHC antigen expression in rat thyroid cells (FRTL-5).
  • To determine the role of intracellular signaling pathways, including cAMP, phosphatidylinositide, and calcium channels, in IFN gamma-induced RT1.B expression.

Main Methods:

  • Immunocytochemistry was used to detect RT1.B antigen expression.
  • FRTL-5 cells were cultured with recombinant rat IFN gamma.
  • Various agents targeting intracellular events, including ionophores, protein kinase inhibitors, and calcium channel blockers, were used.

Main Results:

  • IFN gamma induced RT1.B expression in 88.3% of FRTL-5 cells.
  • TSH deprivation did not affect IFN gamma-induced RT1.B expression.
  • Agents like A23187 and phorbol ester did not induce RT1.B expression.
  • Inhibitors of protein kinase C, calmodulin, and calcium channels did not block IFN gamma-induced RT1.B expression.
  • Cycloheximide inhibited IFN gamma-induced RT1.B expression in a dose-dependent manner, indicating a requirement for de novo protein synthesis.

Conclusions:

  • IFN gamma induces RT1.B antigen expression in FRTL-5 cells.
  • The induction mechanism relies on de novo protein synthesis.
  • The process is independent of the cAMP system, phosphatidylinositide system, and voltage-dependent calcium channels.

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