Experimental allergic encephalomyelitis (EAE) in mice: primary control of EAE susceptibility is outside the H-2 complex.

We report here the results of EAE induction in 1758 mice from 9 inbred strains, 5 H-2 congenic strains, and 6 F1 hybrids. EAE responsiveness is under the primary control of genes outside the H-2 complex. The F1 data do not show a unifactorial inheritance of EAE responsiveness. The F1 data do imply a maternal factor, sex hormone, or sex-linked gene(s) that modifies EAE responsiveness. The data suggest that the H-2 complex modifies the degree of EAE responsiveness. This modulatory effect by H-2 could account for the contradictory reports in the literature on the association of H-2 type and EAE responsiveness.