Autoimmune versus oligodendrogliopathy: The pathogenesis of multiple sclerosis

Jin Nakahara, Sadakazu Aiso, Norihiro Suzuki

Research output: Contribution to journalReview articlepeer-review

17 Citations (Scopus)


Multiple sclerosis (MS) is the most common inflammatory demyelinating disease of the central nervous system (CNS); it affect millions of patients worldwide and the number of patients is on the rise. Current treatment options are fairly limited and there is a strong unmet need for disease-targeted therapies for MS. The most widely accepted hypothesis for the pathogenesis of MS is that it is a primary autoimmune disease in which myelin-specific T cells play a central role in the progression of demyelination. According to this hypothesis, a powerful immune suppression or a reconstruction of the immune system to abrogate disease-specific leukocytes early in the development of the disease is expected to halt or even reverse the disease, since remyelination is an exceptionally efficient regenerative process in the CNS. However, recent neuropathological studies have provided evidence of primary oligodendrogliopathy as a cause of demyelination, suggesting that immune reactions may be a mere secondary event in the course of MS. On the other hand, some recent clinical trial results of new immune-suppressive treatments showed a nearly complete blockade of relapses and significant, albeit incomplete, neurological improvement. Therefore, which hypothesis-autoimmunity or oligodendrogliopathy- lights the correct path to a "cure" for MS?

Original languageEnglish
Pages (from-to)325-333
Number of pages9
JournalArchivum Immunologiae et Therapiae Experimentalis
Issue number5
Publication statusPublished - 2010 Oct


  • Autoimmune
  • Multiple sclerosis
  • Oligodendrogliopathy
  • Pathogenesis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


Dive into the research topics of 'Autoimmune versus oligodendrogliopathy: The pathogenesis of multiple sclerosis'. Together they form a unique fingerprint.

Cite this