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

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.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

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

doi

10.1016/j.jneuroim.2009.01.022

subject

Has Abstract

pub_date

2009-04-30 00:00:00

pages

33-9

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(09)00024-1

journal_volume

209

pub_type

杂志文章

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