Neuroinflammation in multiple sclerosis: evidence for autoimmune dysregulation, not simple autoimmune reaction

Clin Neurol Neurosurg. 2006 Mar;108(3):241-4. doi: 10.1016/j.clineuro.2005.11.006. Epub 2006 Jan 18.


Both inflammatory and neurodegenerative components may contribute to the clinical profile of multiple sclerosis (MS) leading to irreversible deficits when they exceed the threshold of compensation. The mechanisms leading to tissue injury in MS are complex. Inflammation appears to be caused by overactive pro-inflammatory T-helper 1 cells, initiating an inflammatory cascade with several cellular and molecular immune components participating in the pathogenetic mechanism. Current treatments are most effective in the inflammatory phase of the disease since they may interfere with various stages of the immune cascade. Recent evidence has emerged that inflammation may not only be destructive, but may also play a part in tissue repair. This has opened up a new aspect of our knowledge of the role of the inflammatory process in MS. Data regarding the role of regulatory cells in particular, imply that specific immunomodulatory strategies that support the function of these particular cellular subpopulations may participate in the downregulation of autoimmune responses in MS.

Publication types

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

MeSH terms

  • Autoimmunity / physiology*
  • Forkhead Transcription Factors / physiology
  • Humans
  • Inflammation / immunology*
  • Multiple Sclerosis / immunology*
  • Multiple Sclerosis / pathology*
  • Multiple Sclerosis / physiopathology
  • T-Lymphocytes, Regulatory / physiology


  • FOXP3 protein, human
  • Forkhead Transcription Factors