Revisiting the pathoetiology of Multiple Sclerosis : has the tail been wagging the mouse?

Monokesh K. Sen, Mohammed S. M. Almuslehi, Peter J. Shortland, Jens R. Coorssen, David A. Mahns

Research output: Contribution to journalArticlepeer-review

41 Citations (Scopus)

Abstract

Multiple Sclerosis (MS) is traditionally considered an autoimmune-mediated demyelinating disease, the pathoetiology of which is unknown. However, the key question remains whether autoimmunity is the initiator of the disease (outside-in) or the consequence of a slow and as yet uncharacterized cytodegeneration (oligodendrocytosis), which leads to a subsequent immune response (inside-out). Experimental autoimmune encephalomyelitis has been used to model the later stages of MS during which the autoimmune involvement predominates. In contrast, the cuprizone (CPZ) model is used to model early stages of the disease during which oligodendrocytosis and demyelination predominate and are hypothesized to precede subsequent immune involvement in MS. Recent studies combining a boost, or protection, to the immune system with disruption of the blood brain barrier have shown CPZ-induced oligodendrocytosis with a subsequent immune response. In this Perspective, we review these recent advances and discuss the likelihood of an inside-out vs. an outside-in pathoetiology of MS.
Original languageEnglish
Article number572186
Number of pages14
JournalFrontiers in Immunology
Volume11
DOIs
Publication statusPublished - 2020

Open Access - Access Right Statement

© 2020 Sen, Almuslehi, Shortland, Coorssen and Mahns. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY) (https://creativecommons.org/licenses/by/4.0/). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

Keywords

  • central nervous system
  • demyelination
  • encephalomyelitis
  • multiple sclerosis

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