Differing degrees of susceptibility to experimental allergic encephalomyelitis among inbred strains of hamsters.

Susceptibility to experimental allergic encephalomyelitis was examined in five highly inbred strains of hamsters. The frequency of disease was reproducible within a given strain, but differed remarkably from strain to strain. Two strains--Bio 15.16 and Bio 87.20--appeared to share similar major histocompatibility genes. Despite genetic similarities, susceptibility to acute paralytic EAE was remarkably different in the two strains. Strain 15.16 hamsters consistently developed acute paralysis 10-21 days after sensitization with heterologous nervous tissue and immunologic adjuvants. Strain 87.20 hamsters never developed disease acutely. Protection from EAE was not absolute, however, for some animals developed histopathologic evidence of EAE. Using alternative methods to induce EAE did not alter susceptibility in 87.20 hamsters. Genetic analysis of offspring of susceptible 15.16 and resistant 87.20 hamsters suggested that a single autosomal gene, unrelated to the major histocompatibility locus, accounted for differences in EAE susceptibility in these two strains. This gene had a more profound influence on clinical patterns of EAE than on histopathologic markers of disease.