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Glial expression of tumor necrosis factor in transgenic animals: How do these models reflect the “normal situation”?
Author(s) -
Probert Lesley,
Akassoglou Katerina
Publication year - 2001
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.1110
Subject(s) - biology , autoimmunity , tumor necrosis factor alpha , neuroscience , inflammation , transgene , genetically modified mouse , receptor , disease , neurodegeneration , neuroimmunology , immunology , central nervous system , gene , immune system , pathology , genetics , medicine
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‐α (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. GLIA 36:212–219, 2001. © 2001 Wiley‐Liss, Inc.