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.
D000818:Animals; D003433:Crosses, Genetic; D004306:Dose-Response Relationship, Immunologic; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D005260:Female; D006183:H-2 Antigens / Q000235:genetics* / Q000276:immunology; D008285:Major Histocompatibility Complex; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D008811:Mice, Inbred DBA; D008814:Mice, Inbred NZB
D006183:H-2 Antigens