Host expression of IFN-γR determines clinical outcome after adoptive transfer of CNS pathogenic T cells
Mouse genotype . | C57BL6/J . | IFN-γR KO . |
---|---|---|
Incidence of clinical signs | 18/20 | 19/19 |
Incidence of clinical signs of limb dysfunction | 18/20 | 14/19 |
Mean day of onset of clinical limb dysfunction | 7 ± 1 | 10 ± 2 |
Incidence of flaccid paralysis | 18/20 | 0/19 |
Incidence of dystonia | 0/20 | 14/19 |
Mean peak limb dysfunction clinical score | 2.6 ± 1 | 1.2 ± 0.6 |
Incidence of clinical signs of nonclassical EAE | 0/20 | 19/19 |
Mean day of onset of nonclassical signs of EAE | NA | 10 ± 1 |
Vertigo/dysequilibrium | NA | 19/19 |
Ataxia | NA | 19/19 |
Mouse genotype . | C57BL6/J . | IFN-γR KO . |
---|---|---|
Incidence of clinical signs | 18/20 | 19/19 |
Incidence of clinical signs of limb dysfunction | 18/20 | 14/19 |
Mean day of onset of clinical limb dysfunction | 7 ± 1 | 10 ± 2 |
Incidence of flaccid paralysis | 18/20 | 0/19 |
Incidence of dystonia | 0/20 | 14/19 |
Mean peak limb dysfunction clinical score | 2.6 ± 1 | 1.2 ± 0.6 |
Incidence of clinical signs of nonclassical EAE | 0/20 | 19/19 |
Mean day of onset of nonclassical signs of EAE | NA | 10 ± 1 |
Vertigo/dysequilibrium | NA | 19/19 |
Ataxia | NA | 19/19 |
MOG35-55 specific T-cells were generated in C57BL/6 mice and polarized to a Th1 phenotype. The T-cells were then injected IV into either C57BL/6 or IFN-γR–deficient (IFN-γR KO) mice. Mice were examined over time for clinical signs of limb dysfunction, vertigo/disequilibrium, and ataxia. Results shown were pooled from three separate experiments. Results are shown ± SD.