Administration of a monomeric CCL2 variant to EAE mice inhibits inflammatory cell recruitment and protects from demyelination and axonal loss
Copyright policy )Administration of a monomeric CCL2 variant to EAE mice inhibits inflammatory cell recruitment and protects from demyelination and axonal loss
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.
Adult, Male, Encephalomyelitis, Autoimmune, Experimental, Dose-Response Relationship, Drug, Macrophages, T-Lymphocytes, Middle Aged, Mice, Inbred C57BL, Chemotaxis, Leukocyte, Disease Models, Animal, Interferon-gamma, Mice, Neuroprotective Agents, Animals, Humans, Immunologic Factors, Female, Chemokine CCL2, Myelin Sheath, Cell Proliferation
Adult, Male, Encephalomyelitis, Autoimmune, Experimental, Dose-Response Relationship, Drug, Macrophages, T-Lymphocytes, Middle Aged, Mice, Inbred C57BL, Chemotaxis, Leukocyte, Disease Models, Animal, Interferon-gamma, Mice, Neuroprotective Agents, Animals, Humans, Immunologic Factors, Female, Chemokine CCL2, Myelin Sheath, Cell Proliferation
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