Autoimmune-induced preferential depletion of myelin-associated glycoprotein (MAG) is genetically regulated in relapsing EAE (B6 x SJL) F1 mice.

ABSTRACT:

Background

Experimental autoimmune encephalomyelitis (EAE) is commonly used to investigate mechanisms of autoimmune-mediated damage to oligodendrocytes, myelin, and axons in multiple sclerosis (MS). Four distinct autoimmune mechanisms with subsequently distinct patterns of demyelination have been recognized in acute MS lesions. EAE correlates for those distinct patterns of MS lesions are unknown. An excessive loss of myelin-associated glycoprotein (MAG), as a result of distal oligodendrogliopathy, is found exclusively in the subtype III lesion. We sought to answer if types of demyelination in acute lesions during onset and relapse of EAE can replicate the specific patterns observed in MS acute lesions.

Methods

In parental H-2b (C57BL/6, B6) and hybrid H-2b/s [(B6 x SJL) F1]

SUBMITTER: Skundric DS 

PROVIDER: S-EPMC2459167 | biostudies-literature | 2008 Jun

REPOSITORIES: biostudies-literature