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T Cell Depletion on Chemokine and Chemokine Receptor Expression in the Central Nervous System1
*
Department of Pathology and Neuropathology, Albert Einstein College of Medicine, Bronx, NY 10461; and
Scripps Research Institute, La Jolla, CA
Experimental autoimmune encephalomyelitis (EAE) is a demyelinating
disease of the central nervous system (CNS) that is a model for
multiple sclerosis. Previously, we showed that depletion of 
T
cells significantly reduced clinical and pathological signs of disease,
which was associated with reduced expression of IL-1ß, IL-6, TNF-
,
and lymphotoxin at disease onset and a more persistent reduction in
IFN-. In this study, we analyzed the effect of T cell
depletion on chemokine and chemokine receptor expression. In the CNS of
control EAE mice, mRNAs for RANTES, eotaxin, macrophage-inflammatory
protein (MIP)-1, MIP-1ß, MIP-2, inducible protein-10, and monocyte
chemoattractant protein-1 were detected at disease onset, increased as
disease progressed, and fell as clinical signs improved. In T
cell-depleted animals, all of the chemokine mRNAs were reduced at
disease onset; but at the height of disease, expression was variable
and showed no differences from control animals. mRNA levels then fell
in parallel with control EAE mice. ELISA data confirmed reduced
expression of MIP-1 and monocyte chemoattractant protein-1 at
disease onset in T cell-depleted mice, and total T cell numbers
were also reduced. In normal CNS mRNAs for CCR1, CCR3, and CCR5 were
observed, and these were elevated in EAE animals. mRNAs for CCR2 were
also detected in the CNS of affected mice. Depletion of T cells
reduced expression of CCR1 and CCR5 at disease onset only. We conclude
that T cells contribute to the development of EAE by promoting
an inflammatory environment that serves to accelerate the inflammatory
process in the CNS.
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