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Table III.

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.

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