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

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

Research output: Contribution to journalArticlepeer-review

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 IFNγ-releasing effectors T cells. These results suggest that the therapeutic mechanism of P8A-CCL2 may rely on interference with immune cell recruitment.

Original languageEnglish
Pages (from-to)33-39
Number of pages7
JournalJournal of Neuroimmunology
Volume209
Issue number1-2
DOIs
Publication statusPublished - Apr 30 2009

Keywords

  • CCL2
  • CCR2
  • Chemokines
  • EAE/MS

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

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