Abstract：
:The C57BL/6 mice strain is known to be reputedly resistant to induction of experimental autoimmune neuritis (EAN), an animal model of Guillain-Barré syndrome in human by bovine peripheral myelin (BPM), and P2 protein or the P2 protein peptide 57-81. The P0 peptide 180-199 is a stronger neuritogenic antigen than the P2 peptide 57-81. We found that this synthetic peptide induced both clinical and pathological characteristics of an acute monophasic EAN in C57BL/6 mice. Only male mice were more sensitive to EAN induction with the P0 peptide 180-199. Intravenously administrated pertussis toxin (PT) had an adjuvant effect that increased the incidence of P0 peptide 180-199-induced EAN as well as the inflammation and demyelination in the peripheral nerves. Spontaneous and P0 peptide 180-199 stimulated proliferation of peripheral T-cells were enhanced by PT-treatment as well. The enhancing effect was lower before onset of the disease (Day 6 post immunization) (p.i.) as compared to the early phase of the disease (Day 22 p.i.). Thus, P0 peptides together with PT are able to break tolerance to myelin in C57BL/6 mice.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Zou LP,Ljunggren HG,Levi M,Nennesmo I,Wahren B,Mix E,Winblad B,Schalling M,Zhu Jdoi
10.1002/1097-4547(20001201)62:5<717::AID-JNR11>3.0keywords:
subject
Has Abstractpub_date
2000-12-01 00:00:00pages
717-21issue
5eissn
0360-4012issn
1097-4547pii
10.1002/1097-4547(20001201)62:5<717::AID-JNR11>3.0journal_volume
62pub_type
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