Influence of interferon alpha on expression of Fas and Fas ligand in dendritic cells from patients with chronic myeloid leukemia

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2008 Jun;16(3):501-5.

Abstract

The study was aimed to investigate the influence of interferon alpha (IFN-alpha) on the expressions of Fas and Fas ligand (FasL) in dendritic cells (DCs) from patients with chronic myeloid leukemia (CML). In addition to adding stem cell factor (SCF), granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor alpha (TNF-alpha) and interleukin 4 (IL-4), the IFN-alpha was added to the serum-free medium for DCs. After culturing for 10 - 14 days, cell phenotype and percentage of Ph(1) chromosome were detected by different methods. The expression of Fas or FasL on CML-DCs and cell cycle of DCs labeled with propidium iodine (PI) were measured by flow cytometry. The concentration of sFas in supernatants was analyzed by enzyme-linked immunosorbent assay (ELISA). The results indicated that the expression of co-stimulatory molecules were improved significantly while the percentages of Ph(1) positive cells decreased. The level of Fas on cells was up-regulated and the concentration of sFas decreased. However, the expression of FasL was negative. The ratio of apoptosis rose gradually while the concentration of IFN-alpha increased. It is concluded that IFN-alpha can accelerate the apoptosis of Ph(1) positive cells through Fas/FasL pathway, so the number of Ph(1) negative cells increases relatively.

MeSH terms

  • Adolescent
  • Adult
  • Apoptosis / drug effects
  • Cells, Cultured
  • Child
  • Culture Media / pharmacology
  • Dendritic Cells / cytology
  • Dendritic Cells / metabolism*
  • Fas Ligand Protein / genetics
  • Fas Ligand Protein / metabolism*
  • Female
  • Humans
  • Interferon-alpha / pharmacology*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • Male
  • Middle Aged
  • Philadelphia Chromosome
  • Young Adult
  • fas Receptor / genetics
  • fas Receptor / metabolism*

Substances

  • Culture Media
  • Fas Ligand Protein
  • Interferon-alpha
  • fas Receptor