Administration of a monomeric CCL2 variant to EAE mice inhibits inflammatory cell recruitment and protects from demyelination and axonal loss - PubMed (original) (raw)

. 2009 Apr 30;209(1-2):33-9.

doi: 10.1016/j.jneuroim.2009.01.022. Epub 2009 Feb 15.

F Ruffini, A Bergami, E Brambilla, G Dati, B Greco, R Cirillo, A E I Proudfoot, G Comi, R Furlan, P Zaratin, G Martino

Affiliations

• PMID: 19232440
• DOI: 10.1016/j.jneuroim.2009.01.022

Administration of a monomeric CCL2 variant to EAE mice inhibits inflammatory cell recruitment and protects from demyelination and axonal loss

E Brini et al. J Neuroimmunol. 2009.

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.

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