| Type | MGI:General | Description | following immunization with rat rMOG (amino acids 1-125) or with the dominant MOG 35-55 encephalitogenic peptide, homozygotes display no clinical or histological CNS tissue damage, whereas all wild-type controls develop severe EAE following immunization with whole myelin, female homozygotes develop a less severe EAE than wild-type females, as shown by a delayed disease onset (17.9 +/- 6.6 days vs 13.4 days +/- 1.9, respectively), significantly milder clinical signs (mean maximal clinical score 1.5 +/- 1.5 vs 4.4 +/- 1.2), and a reduced mortality rate (15% vs 75%); in male homozygotes, the overall EAE severity is less than that in female homozygotes at day 20 after induction of EAE with whole myelin, homozygotes exhibit a reduced mean clinical score (0.5 vs 2.2), little or no CNS inflammation and no loss of myelin, whereas wild-type controls display clear signs of inflammation and some mild loss of subpial myelin (demyelination) at day 60 after induction of EAE with whole myelin, homozygotes display less meningeal inflammation than wild-type controls (inflammatory index 0.9 +/- 0.5 vs 2.3 +/- 1.0, respectively) and still no evidence of demyelination |
