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

MOG_35-55 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.