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Table II.

IFN-γ production in a fraction of pathogenic T cells prevents development of atypical EAE

Transferred cells
Incidence of nonclassical disease
Incidence of classical EAE
Incidence of both diseases
WT Th1 0/25 21/25 0/25 
IFNγ−/− Th1 22/25 0/25 0/25 
WT Th1 + IFNγ−/− Th1 (1:1) 2/25 24/25 2/25 
OVA Th1 + IFNγ−/− Th1 (1:1) 17/17 0/17 0/17 
WT Th1 + IFNγ−/− Th1 (0.1:1) 11/15 1/15 0/15 
WT Th1 + IFNγ−/− Th1 (0.2:1) 19/30 16/30 6/30 
Transferred cells
Incidence of nonclassical disease
Incidence of classical EAE
Incidence of both diseases
WT Th1 0/25 21/25 0/25 
IFNγ−/− Th1 22/25 0/25 0/25 
WT Th1 + IFNγ−/− Th1 (1:1) 2/25 24/25 2/25 
OVA Th1 + IFNγ−/− Th1 (1:1) 17/17 0/17 0/17 
WT Th1 + IFNγ−/− Th1 (0.1:1) 11/15 1/15 0/15 
WT Th1 + IFNγ−/− Th1 (0.2:1) 19/30 16/30 6/30 

MOG35-55-specific T cell lines were generated in either C57BL/6 (WT) or IFN-γ–deficient (IFN-γ KO) mice and polarized to a Th1 phenotype as described in Materials and methods. Ovalbumin-specific (OVA) T cell lines were also generated in C57BL/6 and polarized to a Th1 phenotype. Mice received either 5 × 106 WT, 5 × 106 IFN-γ KO, 5 × 106 WT and 5 × 106 IFN-γ KO (1:1), 5 × 106 OVA, and 5 × 106 IFN-γ KO cells (1:1), 5 × 105 WT and 5 × 106 IFN-γ KO (0.1:1), or 1 × 106 WT and 5 × 106 IFN-γ KO (0.2:1) as a single i.v. injection. 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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