We have been studying genetic differences in susceptibility to autoimmune encephalomyelitis (EAE) between Strain 13 (susceptible) and Strain 2 (resistant) guinea pigs. Strand 2 sensitized to guinea pig spinal cord antigen shows histological evidence but not clinical signs of EAE. Both genetic and immunological approaches to finding the basis for this difference have been undertaken. Final mortality rates for F2 hybrids were much less than for fully susceptible F1's bringing up the question whether multiple genes are involved in determination of susceptibility to EAE. Adoptive transfer of sensitized T cells to F1 recipients showed that 13 but not 2 donor cells regularly induce clinical disease. Strain 2 lymphocytes can easily transfer tuberculin hypersensitivity and cause histological changes, but not clinical signs without using enormous numbers of donor T cells purified by panning. This indicates a cytotoxic factor capable of damaging neural capacity is in short supply in Strain 2 T cells.
