Administration of a monomeric CCL2 variant to EAE mice inhibits inflammatory cell recruitment and protects from demyelination and axonal loss.
J Neuroimmunol
; 209(1-2): 33-9, 2009 Apr 30.
Article
em En
| MEDLINE
| ID: mdl-19232440
ABSTRACT
Based on gene expression data, we tested the P8A-CCL2 variant of the chemokine CCL2, able to interfere with the chemotactic properties of the parental molecule, in relapsing-remitting (RR)-EAE SJL. Only preventive treatment significantly delayed disease onset in a dose dependent manner. P8A-CCL2 administration, however, decreased demyelination, axonal loss and number of CNS infiltrating T cells and macrophages. Immunological analysis revealed that P8A-CCL2 does not act on Ag-specific T cell proliferation and does not interfere with the differentiation of IFNgamma-releasing effectors T cells. These results suggest that the therapeutic mechanism of P8A-CCL2 may rely on interference with immune cell recruitment.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Quimiotaxia de Leucócito
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Quimiocina CCL2
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Encefalomielite Autoimune Experimental
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Bainha de Mielina
Idioma:
En
Ano de publicação:
2009
Tipo de documento:
Article