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

Autor: Brini E; Neuroimmunology Unit - INSpe, Milan, Italy., Ruffini F, Bergami A, Brambilla E, Dati G, Greco B, Cirillo R, Proudfoot AE, Comi G, Furlan R, Zaratin P, Martino G
Jazyk: angličtina
Zdroj: Journal of neuroimmunology [J Neuroimmunol] 2009 Apr 30; Vol. 209 (1-2), pp. 33-9. Date of Electronic Publication: 2009 Feb 15.
DOI: 10.1016/j.jneuroim.2009.01.022
Abstrakt: 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.
Databáze: MEDLINE
Externí odkaz: