Down-regulation of human tumor necrosis factor-beta gene expression by cells with suppressive activity

Immunol Lett. 1996 Dec;54(2-3):171-6. doi: 10.1016/s0165-2478(96)02668-5.

Abstract

Human TNF-beta (lymphotoxin) gene expression is down-regulated by immunosuppression. Induction of TNF-beta mRNA in lymphoid cells is greatly enhanced by gamma-irradiation, cyclophosphamide and cimetidine, agents that each inhibit activation of suppressive cells. The level of TNF-beta mRNA expressed in response to stimulation, whether by mitogen or antigen, is reduced strongly by concomitant activation of suppressive cell subsets. Removal of CD8 or CD11b cells leads to a pronounced superinduction of TNF-beta mRNA in the depleted cell population. Induction of TNF-beta mRNA precedes appearance of suppressive cell activity, allowing for temporary expression. The TNF-beta gene is as sensitive as IFN-gamma and IL-2 genes to suppression. Hence, three genes characteristically expressed in Th1 cells, encoding IL-2, IFN-gamma, and TNF-beta, are similarly regulated by cell-mediated suppression. Actual levels of TNF-beta during an immune response are determined by the balance between activities of expressing and suppressing cell subsets, both transiently manifested.

MeSH terms

  • CD8 Antigens / immunology
  • Cells, Cultured
  • Cimetidine / pharmacology
  • Cyclophosphamide / pharmacology
  • Down-Regulation*
  • Gamma Rays
  • Gene Expression Regulation*
  • Humans
  • Immunosuppressive Agents / pharmacology
  • Lymphotoxin-alpha / genetics*
  • Macrophage-1 Antigen / immunology

Substances

  • CD8 Antigens
  • Immunosuppressive Agents
  • Lymphotoxin-alpha
  • Macrophage-1 Antigen
  • Cimetidine
  • Cyclophosphamide