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 Neuroimmunoljournal_title
Journal of neuroimmunologyauthors
Smith PA,Morris-Downes M,Heijmans N,Pryce G,Arter E,O'Neill JK,'t Hart B,Baker D,Amor Sdoi
10.1016/j.jneuroim.2005.04.006subject
Has Abstractpub_date
2005-07-01 00:00:00pages
76-84issue
1-2eissn
0165-5728issn
1872-8421pii
S0165-5728(05)00157-8journal_volume
164pub_type
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pub_type: 杂志文章,评审
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