The C57BL/6J mice strain is known to be reputedly resistant to induction of
experimental autoimmune neuritis (EAN), an animal model of Guillain-Barre
syndrome in humans. Here we describe the induction of EAN in mice of the C5
7BL/6J background by transfer into naive syngeneic recipients bovine periph
eral nerve myelin (BPM)-primed donor lymph node cells that had been stimula
ted in vitro with the bovine peripheral nervous system (PNS) myelin P2 prot
ein peptide 57-81 followed by challenge with BPM, Freund's complete adjuvan
t and pertussis toxin. EAN was more severe, both clinically and histologica
lly, and accompanied by extensive infiltration of inflammatory cells and de
myelination in peripheral nerves when examined on day 30 after transfer of
primed T cells from CD4(-)8(-) mice into identical naive hosts than after t
ransfer of cells from primed wild type, CD4(-)/(-) or CD8(-)/(-) mice to co
rresponding recipient animals. EAN in CD4(-)8(-) mice was also associated w
ith elevated numbers of P2 peptide-reactive interferon-gamma (IFN-gamma) se
creting cells and alpha beta T cells were present in lymph nodes and spleen
s. The data suggest that PNS myelin activated T cells from an EAN-resistant
mice strain are capable of homing to the PNS. The expanded CD4(-)8(-) alph
a beta T cells may have helper and effector functions, related to initiatio
n of EAN in the CD4(-)8(-) mice. Lack of CD4(+) and CD8(+) expressing cells
does not prevent the initiation of an autoimmune disease. (C) 1999 Elsevie
r Science B.V. All rights reserved.