Activation of class I HLA expression by TNF-alpha and gamma-interferon is mediated through protein kinase C-dependent pathway in CML cell lines

Br J Haematol. 1991 Jul;78(3):359-67. doi: 10.1111/j.1365-2141.1991.tb04449.x.

Abstract

The combination of tumour necrosis factor alpha (TNF alpha) and gamma-interferon induced transcription of class I HLA genes in chronic myelogenous leukaemia (CML) cell lines through the formation of a complex between nuclear proteins and the transcriptional enhancers associated with these genes. Although gamma-interferon or TNF-alpha stimulated expression of class I HLA antigens in the EM2 and K562 CML cell lines when used alone, the effect of the combination of TNF-alpha and gamma-interferon was greater than that observed with either agent alone. The induction of class I HLA expression by gamma-interferon and TNF-alpha was inhibited completely by the isoquinoline sulfonamide H7, an inhibitor of protein kinase C. We conclude that the enhancement of the gamma-interferon induced transcriptional activation of class I HLA gene expression by TNF-alpha involves a protein kinase C-dependent pathway.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Base Sequence
  • Cell Division
  • Cell Line
  • Enhancer Elements, Genetic
  • Gene Expression
  • Genes, MHC Class I / drug effects*
  • Interferon-gamma / pharmacology*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • Molecular Sequence Data
  • Nuclear Proteins / metabolism
  • Protein Kinase C / metabolism
  • RNA, Messenger / analysis
  • Transcription, Genetic / drug effects*
  • Tumor Cells, Cultured / drug effects
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Nuclear Proteins
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma
  • Protein Kinase C