Glial expression of tumor necrosis factor in transgenic animals: how do these models reflect the "normal situation"?

Glia. 2001 Nov;36(2):212-9. doi: 10.1002/glia.1110.


Recent progress in the field of experimental genetics, which enables the selective and conditional ablation or dysregulation in the expression of specific genes in mice, and its application to the study of experimentally inducible models for human disease, have contributed enormously to our understanding of the molecules and mechanisms that underlie autoimmunity and inflammation in the CNS. This article describes the lessons learned from the application of such technology to the study of the tumor necrosis factor-alpha (TNF) ligand/receptor system in the CNS. Important roles for TNF and its two membrane-bound receptors in the initiation and support of CNS inflammation, the development of CNS autoimmunity, and possibly in the resolution of T-cell-mediated disease, as well as their implications for our understanding of the "normal" cellular and molecular mechanisms that underlie CNS pathology, are discussed.

Publication types

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

MeSH terms

  • Animals
  • Animals, Genetically Modified / immunology*
  • Central Nervous System / immunology*
  • Disease Models, Animal
  • Encephalitis / immunology*
  • Humans
  • Multiple Sclerosis / drug therapy
  • Multiple Sclerosis / immunology
  • Multiple Sclerosis / physiopathology
  • Neuroglia / immunology*
  • Tumor Necrosis Factor-alpha / immunology*
  • Tumor Necrosis Factor-alpha / physiology


  • Tumor Necrosis Factor-alpha