Analysis Tools
immune system
| N |
• both homozygous mutant and wild-type mice display similar T and B cell responses against the extracellular domain of MOG, including the immunodominant MOG 35-55 T cell epitope
• no differences in secondary in vitro T cell-proliferative responses to rMOG or to an overlapping set of 31 mouse MOG peptides are observed between wild-type and homozygous mutant mice
• upon adoptive transfer, MOG-specific T cells from homozygous mutant mice and wild-type mice show an equal encephalitogenic potential, regardless of whether preactivated MOG-specific T cells or undifferentiated resting T cells are transferred
• collectively, these data imply that wild-type control mice do not develop detectable immune tolerance to MOG
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• 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
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nervous system
| N |
• at 2-, 4-, and 14 months of age, homozygotes display a normal myelin sheath architecture in the corpus callosum, striatum, cerebellum, and optic nerve relative to wild-type controls
• no differences in myelin sheath compaction, myelination kinetics or axonal structure are observed
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