B-Cell activity in weanling Lewis rats was inhibited by injections of goat anti-rat mu-chain antiserum (GAMS) from birth on, as demonstrated by markedly reduced or absent myelin basic protein (MBP) binding activity of sera. Following challenge with guinea pig spinal cord (GPSC)-complete Freund's adjuvant (CFA) and continued GAMS treatment, all rats remained clinically well without a trace of neurological signs. Histopathologically, central nervous system (CNS) perivascular fibrin deposits, typically accompanying paralytic signs of the disease, were virtually absent in GAMS-treated rats, despite occurrence of perivascular cell infiltrates of variable degrees of severity. In addition, preliminary studies of plastic embedded tissues suggest that demyelination is appreciably reduced in GAMS-treated and challenged rats. In contrast, control littermates similarly treated with normal goat serum (NGS) or normal goat IgG (NGIgG) and challenged, developed typical paralytic signs and perivascular fibrin deposits characteristic focal perivascular cellular infiltrates and demyelination of EAE, as well as anti-MBP antibodies.
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