CNS expression of EAE-associated inflammatory proteins changes in the absence of an IFN-γ signal MOG35-55-specific T cell lines were generated in either C57BL/6 or IFN-γ–deficient mice and polarized to a Th1 phenotype. T cells were injected IV into either C57BL/6 or IFN-γR–deficient mice at 1 × 107 cells/mouse. Between 24 and 48 h after disease onset, mRNA was extracted from spinal cord and cerebellum and examined for inflammatory expression patterns using real time PCR as described in Materials and methods. Moderate Th1 tissue was extracted from animals that exhibited classical clinical scores of 1–2 in the 24–48 h after onset. Severe Th1 tissue was extracted from mice that exhibited classical clinical scores of 2.5–3.5 during the same period. The cells used to induce the severe EAE were injected in parallel into IFN-γR–deficient mice (IFN-γR null). The tissue in the IFN-γ–null group was extracted from WT mice that received IFN-γ–deficient pathogenic T cells. The data are presented as mean ± SEM of 4–5 mice/group from two independent experiments.
