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,§
,§
Departments of
*
Neurology and
Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland, OR 97201;
L. Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland; and
§
Neuroimmunology Research, Veterans Affairs Medical Center, Portland, OR 97201
The perivascular transmigration and accumulation of macrophages and
T lymphocytes in the CNS of mice with experimental autoimmune
encephalomyelitis (EAE) may be partly regulated by low m.w. chemotactic
cytokines. Using the RNase protection assay and ELISA, we quantified
expression of chemokines and chemokine receptors in the spinal cord
(SC), brain, and lymph nodes of BV8S2 transgenic mice that developed or
were protected from EAE by vaccination with BV8S2 protein. In paralyzed
control mice, the SC had increased cellular infiltration and strong
expression of the chemokines RANTES, IFN-inducible 10-kDa protein, and
monocyte chemoattractant protein-1 and the cognate chemokine receptors
CCR1, CCR2, and CCR5, with lower expression of macrophage-inflammatory
protein (MIP)-1
, MIP-1ß, and MIP-2; whereas brain had less
infiltration and a lower expression of a different pattern of
chemokines and receptors. In TCR-protected mice, there was a decrease
in the number of inflammatory cells in both SC and brain. In SC, the
reduced cellular infiltrate afforded by TCR vaccination was
commensurate with profoundly reduced expression of chemokines and their
cognate chemokine receptors. In brain, however, TCR vaccination did not
produce significant changes in chemokine expression but resulted in an
increased expression of CCR3 and CCR4 usually associated with Th2
cells. In contrast to CNS, lymph nodes of protected mice had a
significant increase in expression of MIP-2 and MIP-1ß but no change
in expression of chemokine receptors. These results demonstrate that
TCR vaccination results in selective reduction of inflammatory
chemokines and chemokine receptors in SC, the target organ most
affected during EAE.
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