J Autoimmun 2002 Dec;19(4):195-201
Lyons JA, Ramsbottom MJ, Trotter JL, Cross AH.
Department of Neurology and Neurosurgery, Washington University School
of Medicine, St. Louis, MO, USA
It was previously shown that BALB/c mice were susceptible to experimental autoimmune encephalomyelitis induced by immunization with proteolipid protein (PLP).
To determine the encephalitogenic epitopes of PLP in BALB/c mice, mice were immunized with successively smaller pools of 20-mer peptides spanning the PLP molecule from amino acid 30 to amino acid 206.
Immunization with PLP(180-199) resulted in clinical EAE in 9/15 mice (mean max clinical score of 3.3), and immunization with PLP(185-206) induced clinical EAE in 7/21 BALB/c mice (mean maximum score of 3.7).
No relapses in disease were observed.
No EAE was observed in BALB/c mice immunized with PLP(185-199) (n=15), PLP(178-191) (n=13) or other regions of PLP (n=15).
Passive transfer of PLP(180-199)-primed lymph node cells into nai;ve BALB/c mice resulted in EAE (2/2 mice, max score of 4.0).
One-micron toluidine blue stained sections from the spinal cord of EAE-affected BALB/c mice revealed features typical of EAE in other strains, including mononuclear cell infiltration, myelin loss, and axonal loss.