Epitope spread is not critical for the relapse and progression of MOG 8-21 induced EAE in Biozzi ABH mice.

Abstract:

:Emerging autoimmunity (epitope-spreading) generated as a consequence of myelin damage is suggested to underlie the relapses in multiple sclerosis (MS). Myelin oligodendrocyte glycoprotein (MOG 8-21) induces relapsing EAE in ABH mice characterized by broadening of the autoimmune reportoire. Despite epitope spreading tolerance to the priming antigen, but not emerging epitope reactivities, resulted in long-term inhibition of clinical relapse. In contrast, spinal cord homogenate induced EAE was dominated by a proteolipid protein (PLP 56-70) autoreactivity despite the plethora of CNS antigens in the immunogen. This data suggests that during relapsing-remitting demyelinating disease the pathogenic process is dominated by the initiating antigen, with only a minor role played by emerging T-cell populations. These findings may have important implications for the efficacy of antigen-based immune therapies in autoimmune disorders.

journal_name

J Neuroimmunol

authors

Smith PA,Morris-Downes M,Heijmans N,Pryce G,Arter E,O'Neill JK,'t Hart B,Baker D,Amor S

doi

10.1016/j.jneuroim.2005.04.006

subject

Has Abstract

pub_date

2005-07-01 00:00:00

pages

76-84

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(05)00157-8

journal_volume

164

pub_type

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