Glatiramer acetate reduces Th-17 inflammation and induces regulatory T-cells in the CNS of mice with relapsing-remitting or chronic EAE

Rina Aharoni; Raya Eilam; Ariel Stock; Anya Vainshtein; Elias Shezen; Hilah Gal; Nir Friedman; Ruth Arnon

doi:10.1016/j.jneuroim.2010.04.022

Glatiramer acetate reduces Th-17 inflammation and induces regulatory T-cells in the CNS of mice with relapsing-remitting or chronic EAE

Rina Aharoni, Raya Eilam, Ariel Stock, Anya Vainshtein, Elias Shezen, Hilah Gal, Nir Friedman, Ruth Arnon^*

^*Corresponding author for this work

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

69 Scopus citations

Abstract

The aim of this study was to identify cell populations relevant to pathogenesis and repair within the injured CNS in mice that recovered from experimental autoimmune encephalomyelitis (EAE). We demonstrate that in two EAE models, with either relapsing-remitting or chronic course, T-cells and resident activated microglia manifested extensive IL-17 expression, with apparent localization within regions of myelin loss. In mice treated with glatiramer acetate (GA, Copaxone®), even when treatment started after disease exacerbation, CNS inflammation and Th-17 occurrence were drastically reduced, with parallel elevation in T-regulatory cells, indicating the immunomodulatory therapeutic consequences of GA treatment in situ.

Original language	American English
Pages (from-to)	100-111
Number of pages	12
Journal	Journal of Neuroimmunology
Volume	225
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2010.04.022
State	Published - Aug 2010
Externally published	Yes

Bibliographical note

Funding Information:
This study was supported by a grant from Teva Pharmaceutical Industries (Israel), by a grant from the International Human Frontier Science Program Organization, and by a grant from the Israel Science Foundation (grant No. 812/08). N.F. is incumbent of the Pauline Recanati career development chair. We thank Dr. Ilan Volovitz for his help in the spinal cord cell isolation, Dr. Shlomit Reich-Zeliger for her help with multicolor FACS experiments, Dr. Yaron Antebi for help with FACS data analysis, Mrs. Veronique Amor for help in the IVIS experiments and Mrs. Haya Avital for the graphic work.

Keywords

Experimental autoimmune encephalomyelitis
Glatiramer acetate
Immunomodulation
Interleukin-17
Multiple sclerosis
T-regulatory cells

Access to Document

10.1016/j.jneuroim.2010.04.022

Cite this

@article{a8e5f54ab98c4f32926e00d230bb9663,

title = "Glatiramer acetate reduces Th-17 inflammation and induces regulatory T-cells in the CNS of mice with relapsing-remitting or chronic EAE",

abstract = "The aim of this study was to identify cell populations relevant to pathogenesis and repair within the injured CNS in mice that recovered from experimental autoimmune encephalomyelitis (EAE). We demonstrate that in two EAE models, with either relapsing-remitting or chronic course, T-cells and resident activated microglia manifested extensive IL-17 expression, with apparent localization within regions of myelin loss. In mice treated with glatiramer acetate (GA, Copaxone{\textregistered}), even when treatment started after disease exacerbation, CNS inflammation and Th-17 occurrence were drastically reduced, with parallel elevation in T-regulatory cells, indicating the immunomodulatory therapeutic consequences of GA treatment in situ.",

keywords = "Experimental autoimmune encephalomyelitis, Glatiramer acetate, Immunomodulation, Interleukin-17, Multiple sclerosis, T-regulatory cells",

author = "Rina Aharoni and Raya Eilam and Ariel Stock and Anya Vainshtein and Elias Shezen and Hilah Gal and Nir Friedman and Ruth Arnon",

note = "Funding Information: This study was supported by a grant from Teva Pharmaceutical Industries (Israel), by a grant from the International Human Frontier Science Program Organization, and by a grant from the Israel Science Foundation (grant No. 812/08). N.F. is incumbent of the Pauline Recanati career development chair. We thank Dr. Ilan Volovitz for his help in the spinal cord cell isolation, Dr. Shlomit Reich-Zeliger for her help with multicolor FACS experiments, Dr. Yaron Antebi for help with FACS data analysis, Mrs. Veronique Amor for help in the IVIS experiments and Mrs. Haya Avital for the graphic work.",

year = "2010",

month = aug,

doi = "10.1016/j.jneuroim.2010.04.022",

language = "American English",

volume = "225",

pages = "100--111",

journal = "Journal of Neuroimmunology",

issn = "0165-5728",

publisher = "Elsevier",

number = "1-2",

}

TY - JOUR

T1 - Glatiramer acetate reduces Th-17 inflammation and induces regulatory T-cells in the CNS of mice with relapsing-remitting or chronic EAE

AU - Aharoni, Rina

AU - Eilam, Raya

AU - Stock, Ariel

AU - Vainshtein, Anya

AU - Shezen, Elias

AU - Gal, Hilah

AU - Friedman, Nir

AU - Arnon, Ruth

N1 - Funding Information: This study was supported by a grant from Teva Pharmaceutical Industries (Israel), by a grant from the International Human Frontier Science Program Organization, and by a grant from the Israel Science Foundation (grant No. 812/08). N.F. is incumbent of the Pauline Recanati career development chair. We thank Dr. Ilan Volovitz for his help in the spinal cord cell isolation, Dr. Shlomit Reich-Zeliger for her help with multicolor FACS experiments, Dr. Yaron Antebi for help with FACS data analysis, Mrs. Veronique Amor for help in the IVIS experiments and Mrs. Haya Avital for the graphic work.

PY - 2010/8

Y1 - 2010/8

N2 - The aim of this study was to identify cell populations relevant to pathogenesis and repair within the injured CNS in mice that recovered from experimental autoimmune encephalomyelitis (EAE). We demonstrate that in two EAE models, with either relapsing-remitting or chronic course, T-cells and resident activated microglia manifested extensive IL-17 expression, with apparent localization within regions of myelin loss. In mice treated with glatiramer acetate (GA, Copaxone®), even when treatment started after disease exacerbation, CNS inflammation and Th-17 occurrence were drastically reduced, with parallel elevation in T-regulatory cells, indicating the immunomodulatory therapeutic consequences of GA treatment in situ.

AB - The aim of this study was to identify cell populations relevant to pathogenesis and repair within the injured CNS in mice that recovered from experimental autoimmune encephalomyelitis (EAE). We demonstrate that in two EAE models, with either relapsing-remitting or chronic course, T-cells and resident activated microglia manifested extensive IL-17 expression, with apparent localization within regions of myelin loss. In mice treated with glatiramer acetate (GA, Copaxone®), even when treatment started after disease exacerbation, CNS inflammation and Th-17 occurrence were drastically reduced, with parallel elevation in T-regulatory cells, indicating the immunomodulatory therapeutic consequences of GA treatment in situ.

KW - Experimental autoimmune encephalomyelitis

KW - Glatiramer acetate

KW - Immunomodulation

KW - Interleukin-17

KW - Multiple sclerosis

KW - T-regulatory cells

UR - http://www.scopus.com/inward/record.url?scp=77955658134&partnerID=8YFLogxK

U2 - 10.1016/j.jneuroim.2010.04.022

DO - 10.1016/j.jneuroim.2010.04.022

M3 - Article

C2 - 20554028

AN - SCOPUS:77955658134

SN - 0165-5728

VL - 225

SP - 100

EP - 111

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

IS - 1-2

ER -

Glatiramer acetate reduces Th-17 inflammation and induces regulatory T-cells in the CNS of mice with relapsing-remitting or chronic EAE

Abstract

Bibliographical note

Keywords

Access to Document

Other files and links

Fingerprint

Cite this