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  • Title: Administration of a monomeric CCL2 variant to EAE mice inhibits inflammatory cell recruitment and protects from demyelination and axonal loss.
    Author: Brini E, Ruffini F, Bergami A, Brambilla E, Dati G, Greco B, Cirillo R, Proudfoot AE, Comi G, Furlan R, Zaratin P, Martino G.
    Journal: J Neuroimmunol; 2009 Apr 30; 209(1-2):33-9. PubMed ID: 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.
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