Role of interferons in demyelinating diseases

J Neural Transm Suppl. 1997;49:117-23. doi: 10.1007/978-3-7091-6844-8_13.

Abstract

IFN beta-1b reduces the frequency of major multiple sclerosis attacks by 50 percent. Serial MRI scanning over the course of the clinical trial that led to approval of the agent revealed a significant lessening both in disease activity and in accumulating burden of disease in IFN beta-1b-treated patients compared to placebo-treated controls. The mechanism by which IFN beta-1b exerts its beneficial effect in multiple sclerosis is unknown. T suppressor cell function fails during MS attacks and is persistently subnormal in multiple sclerosis patients with progressive disease. IFN beta-1b partially restores suppressor function in multiple sclerosis patients. IFN beta-1b also inhibits release of lymphotoxin, tumor necrosis factor, and interferon gamma, at least in vitro. All three cytokines are toxic to oligodendrocytes. In contrast; production of transforming growth factor beta-1 (TGF beta 1) is increased by IFN beta-1b. TGF beta 1 is an immunosuppressive cytokine. All of the above listed actions of IFN beta-1b could contribute to its beneficial effect. Perhaps all do.

Publication types

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

MeSH terms

  • Demyelinating Diseases / immunology*
  • Demyelinating Diseases / pathology
  • Demyelinating Diseases / therapy*
  • Humans
  • Interferon beta-1a
  • Interferon beta-1b
  • Interferon-beta / therapeutic use*
  • Interferon-gamma / biosynthesis
  • Interferon-gamma / physiology*
  • Magnetic Resonance Imaging
  • Multiple Sclerosis / immunology*
  • Multiple Sclerosis / pathology
  • Multiple Sclerosis / therapy*
  • Recombinant Proteins / therapeutic use
  • Transforming Growth Factor beta / biosynthesis

Substances

  • Recombinant Proteins
  • Transforming Growth Factor beta
  • Interferon beta-1b
  • Interferon-beta
  • Interferon-gamma
  • Interferon beta-1a