Positive and negative implications of tumor necrosis factor neutralization for the pathogenesis of multiple sclerosis

Neurodegener Dis. 2008;5(1):32-7. doi: 10.1159/000109936.

Abstract

Multiple sclerosis (MS) is a progressive, presumably autoimmune, degenerative disease of the central nervous system (CNS). The mechanisms which trigger the disease are unknown, but the pathology of MS is caused by the host's own immune system, which invades the CNS and attacks the myelin sheath that protects and insulates the axons of the nerve cells. Although this inflammatory assault selectively destroys myelin, it is believed that the neurological deficits of MS are rather the consequence of damage to axons, which occurs secondary to inflammation. The inflammatory mediators are generally secreted by myelin-specific, CD4+ T cells, CD8+ T cells, macrophages and activated glial cells and include a large number of cytokines, chemokines and other proinflammatory proteins.

Publication types

  • Review

MeSH terms

  • Animals
  • Antibodies, Monoclonal / immunology
  • Antibodies, Monoclonal / pharmacology
  • Autoantibodies / drug effects
  • Autoantibodies / immunology
  • Humans
  • Immunologic Factors / immunology*
  • Immunologic Factors / pharmacology*
  • Inflammation Mediators / antagonists & inhibitors
  • Inflammation Mediators / immunology
  • Leukocytes / drug effects
  • Leukocytes / immunology
  • Multiple Sclerosis / drug therapy*
  • Multiple Sclerosis / immunology*
  • Multiple Sclerosis / physiopathology
  • Myelin Sheath / drug effects
  • Myelin Sheath / immunology
  • Myelin Sheath / pathology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / immunology*
  • Wallerian Degeneration / drug therapy
  • Wallerian Degeneration / immunology
  • Wallerian Degeneration / physiopathology

Substances

  • Antibodies, Monoclonal
  • Autoantibodies
  • Immunologic Factors
  • Inflammation Mediators
  • Tumor Necrosis Factor-alpha