Home > Journals > Minerva Medica > Past Issues > Minerva Medica 2008 April;99(2) > Minerva Medica 2008 April;99(2):119-40

CURRENT ISSUE
 

JOURNAL TOOLS

eTOC
To subscribe PROMO
Submit an article
Recommend to your librarian
 

ARTICLE TOOLS

Reprints
Permissions

 

MULTIPLE SCLEROSIS   

Minerva Medica 2008 April;99(2):119-40

Copyright © 2008 EDIZIONI MINERVA MEDICA

language: English

The immunology of multiple sclerosis: disease mechanisms and therapeutic targets

Holmøy T. 1, 2

1 Institute of Immunology Rikshospitalet University Hospital Faculty of Medicine, University of Oslo Oslo, Norway 2 Department of Neurology Ullevål University Hospital Oslo, Norway


PDF


The disease mechanism of multiple sclerosis (MS) involves inflammation, demyelination and neurodegeneration. The relation between these components is not completely understood, but recent experiences with aggressive anti-inflammatory treatment suggest that inflammation drives neuronal damage in patients with relapsing remitting MS. Although infiltration of lymphocytes into the brain parenchyma was recognized as a key event in the pathogenesis of MS more than 120 years ago, important aspects of the mechanisms triggering and sustaining this immune response remain unknown. Furthermore, studies of MS lesions and evidence from therapeutic trials suggest that the disease mechanism may vary both throughout the disease course and between patients. The understanding of MS as an autoimmune disease targeting myelin proteins is shaped by the animal model experimental autoimmune encephalomyelitis (EAE), but translation from EAE to MS has proven to be difficult. Although both the EAE model and the prominent association to HLA class II molecules suggest a key role for CD4+ T helper cells, it is not known if or how their tolerance to myelin proteins or other putative autoantigens are broken in MS. This paper reviews some important concepts and controversies in the understanding of the immunological basis for MS and its treatment.

top of page