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T Cell Depletion on Cytokine Gene Expression in Experimental Allergic Encephalomyelitis1
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461
In experimental autoimmune encephalomyelitis (EAE), a model for
multiple sclerosis, we showed previously that depletion of 
T
cells using the mAb GL3 immediately before disease onset, or during the
chronic phase, significantly ameliorated clinical severity. We now
report on the effect of T cell depletion on expression of five
cytokine genes, IL-1, IL-6, TNF, lymphotoxin, and IFN- in spinal
cords of mice during the pre-onset, onset, height, and recovery phases
of EAE, and on expression of type II nitric oxide synthase. In control
animals, the mRNAs for IL-1 and IL-6 rose dramatically at disease onset
and peaked before disease height, whereas the mRNAs for TNF,
lymphotoxin, and IFN- rose more slowly and peaked with peak of
disease. In GL3-treated animals, a dramatic reduction in all five
cytokines was noted at disease onset, but only IFN- remained
significantly reduced at a time point equivalent to height of disease
in control animals. ELISA data confirmed the reduced levels of IL-1 and
IL-6 at disease onset in GL3-treated animals, and pathologic analysis
demonstrated a marked reduction in meningeal infiltrates at the same
time point. Studies of type II NOS also demonstrated a significant
reduction in both mRNA and protein expression at the height of disease
in GL3-treated animals. These results suggest that T cells
contribute to the pathogenesis of EAE by regulating the influx of
inflammatory cells into the spinal cord and by augmenting the
proinflammatory cytokine profile of the inflammatory infiltrates.
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