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

doi:10.1016/j.jneuroim.2009.01.022

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

IRCCS Ospedale San Raffaele

Research output: Contribution to journal › Article › peer-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 language	English
Pages (from-to)	33-39
Number of pages	7
Journal	Journal of Neuroimmunology
Volume	209
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2009.01.022
Publication status	Published - Apr 30 2009

Keywords

CCL2
CCR2
Chemokines
EAE/MS

ASJC Scopus subject areas

Immunology
Clinical Neurology
Immunology and Allergy
Neurology

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10.1016/j.jneuroim.2009.01.022

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Brini, E., Ruffini, F., Bergami, A., Brambilla, E., Dati, G., Greco, B., Cirillo, R., Proudfoot, A. E. I., Comi, G., Furlan, R., Zaratin, P., & Martino, G. (2009). Administration of a monomeric CCL2 variant to EAE mice inhibits inflammatory cell recruitment and protects from demyelination and axonal loss. Journal of Neuroimmunology, 209(1-2), 33-39. https://doi.org/10.1016/j.jneuroim.2009.01.022

Administration of a monomeric CCL2 variant to EAE mice inhibits inflammatory cell recruitment and protects from demyelination and axonal loss. / Brini, E.; Ruffini, F.; Bergami, A.; Brambilla, E.; Dati, G.; Greco, B.; Cirillo, R.; Proudfoot, A. E I; Comi, G.; Furlan, R.; Zaratin, P.; Martino, G.

In: Journal of Neuroimmunology, Vol. 209, No. 1-2, 30.04.2009, p. 33-39.

Research output: Contribution to journal › Article › peer-review

Brini, E, Ruffini, F, Bergami, A, Brambilla, E, Dati, G, Greco, B, Cirillo, R, Proudfoot, AEI, Comi, G , Furlan, R, Zaratin, P & Martino, G 2009, 'Administration of a monomeric CCL2 variant to EAE mice inhibits inflammatory cell recruitment and protects from demyelination and axonal loss', Journal of Neuroimmunology, vol. 209, no. 1-2, pp. 33-39. https://doi.org/10.1016/j.jneuroim.2009.01.022

Brini, E. ; Ruffini, F. ; Bergami, A. ; Brambilla, E. ; Dati, G. ; Greco, B. ; Cirillo, R. ; Proudfoot, A. E I ; Comi, G. ; Furlan, R. ; Zaratin, P. ; Martino, G. / Administration of a monomeric CCL2 variant to EAE mice inhibits inflammatory cell recruitment and protects from demyelination and axonal loss. In: Journal of Neuroimmunology. 2009 ; Vol. 209, No. 1-2. pp. 33-39.

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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.",

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AU - Ruffini, F.

AU - Bergami, A.

AU - Brambilla, E.

AU - Dati, G.

AU - Greco, B.

AU - Cirillo, R.

AU - Proudfoot, A. E I

AU - Comi, G.

AU - Furlan, R.

AU - Zaratin, P.

AU - Martino, G.

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AB - 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.

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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

Keywords

ASJC Scopus subject areas

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