Recent insights into the mechanism of action of glatiramer acetate

Mrinalini Kala; Augusto Miravalle; Timothy Vollmer

doi:10.1016/j.jneuroim.2011.01.009

Recent insights into the mechanism of action of glatiramer acetate

Mrinalini Kala
, Augusto Miravalle
, Timothy Vollmer

COM Phx Internal Medicine

Research output: Contribution to journal › Review article › peer-review

55 Scopus citations

Abstract

Glatiramer acetate (GA, Copaxone®, co-polymer 1) is an immunomodulatory therapy approved in 1996 by the United States Food and Drug Administration for treatment of relapsing-remitting multiple sclerosis. GA has a good safety profile, moderate efficacy, and a unique mode of action. Recent evidence in an animal model of MS, experimental autoimmune encephalomyelitis (EAE), suggests that GA effects on NK cells and B cells may contribute to therapeutic efficacy. We review the mechanism of action of GA, with particular focus on recent data suggesting a role for regulatory B cells.

Original language	English (US)
Pages (from-to)	9-17
Number of pages	9
Journal	Journal of Neuroimmunology
Volume	235
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2011.01.009
State	Published - Jun 2011

Keywords

B cells
Glatiramer acetate
Multiple sclerosis

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

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10.1016/j.jneuroim.2011.01.009

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@article{8aa4a4c559aa487aa892f9a640343304,

title = "Recent insights into the mechanism of action of glatiramer acetate",

abstract = "Glatiramer acetate (GA, Copaxone{\textregistered}, co-polymer 1) is an immunomodulatory therapy approved in 1996 by the United States Food and Drug Administration for treatment of relapsing-remitting multiple sclerosis. GA has a good safety profile, moderate efficacy, and a unique mode of action. Recent evidence in an animal model of MS, experimental autoimmune encephalomyelitis (EAE), suggests that GA effects on NK cells and B cells may contribute to therapeutic efficacy. We review the mechanism of action of GA, with particular focus on recent data suggesting a role for regulatory B cells.",

keywords = "B cells, Glatiramer acetate, Multiple sclerosis",

author = "Mrinalini Kala and Augusto Miravalle and Timothy Vollmer",

note = "Funding Information: Research work in Dr Kala's lab is supported by a grant from Arizona Biomedical Research Commission and Barrow Neurological Foundation . We thank Pippa Loupe, PhD (Teva Pharmaceuticals, Kansas City, MO) for her support and Sheila Truten, B.S. (Medical Communication Company., Philadelphia, PA) for editing the manuscript. We like to thank Jamie L. Canales (Neuroscience publication, Barrow Neurological Institute, Phoenix, AZ) for editing the figures. We also like to thank Dawn Mutchler (Neuroscience publication, Barrow Neurological Institute, Phoenix, AZ) for her support.",

year = "2011",

month = jun,

doi = "10.1016/j.jneuroim.2011.01.009",

language = "English (US)",

volume = "235",

pages = "9--17",

journal = "Journal of Neuroimmunology",

issn = "0165-5728",

publisher = "Elsevier B.V.",

number = "1-2",

}

TY - JOUR

T1 - Recent insights into the mechanism of action of glatiramer acetate

AU - Kala, Mrinalini

AU - Miravalle, Augusto

AU - Vollmer, Timothy

N1 - Funding Information: Research work in Dr Kala's lab is supported by a grant from Arizona Biomedical Research Commission and Barrow Neurological Foundation . We thank Pippa Loupe, PhD (Teva Pharmaceuticals, Kansas City, MO) for her support and Sheila Truten, B.S. (Medical Communication Company., Philadelphia, PA) for editing the manuscript. We like to thank Jamie L. Canales (Neuroscience publication, Barrow Neurological Institute, Phoenix, AZ) for editing the figures. We also like to thank Dawn Mutchler (Neuroscience publication, Barrow Neurological Institute, Phoenix, AZ) for her support.

PY - 2011/6

Y1 - 2011/6

N2 - Glatiramer acetate (GA, Copaxone®, co-polymer 1) is an immunomodulatory therapy approved in 1996 by the United States Food and Drug Administration for treatment of relapsing-remitting multiple sclerosis. GA has a good safety profile, moderate efficacy, and a unique mode of action. Recent evidence in an animal model of MS, experimental autoimmune encephalomyelitis (EAE), suggests that GA effects on NK cells and B cells may contribute to therapeutic efficacy. We review the mechanism of action of GA, with particular focus on recent data suggesting a role for regulatory B cells.

AB - Glatiramer acetate (GA, Copaxone®, co-polymer 1) is an immunomodulatory therapy approved in 1996 by the United States Food and Drug Administration for treatment of relapsing-remitting multiple sclerosis. GA has a good safety profile, moderate efficacy, and a unique mode of action. Recent evidence in an animal model of MS, experimental autoimmune encephalomyelitis (EAE), suggests that GA effects on NK cells and B cells may contribute to therapeutic efficacy. We review the mechanism of action of GA, with particular focus on recent data suggesting a role for regulatory B cells.

KW - B cells

KW - Glatiramer acetate

KW - Multiple sclerosis

UR - https://www.scopus.com/pages/publications/79958007082

UR - https://www.scopus.com/pages/publications/79958007082#tab=citedBy

U2 - 10.1016/j.jneuroim.2011.01.009

DO - 10.1016/j.jneuroim.2011.01.009

M3 - Review article

C2 - 21402415

AN - SCOPUS:79958007082

SN - 0165-5728

VL - 235

SP - 9

EP - 17

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

IS - 1-2

ER -

Recent insights into the mechanism of action of glatiramer acetate

Abstract

Keywords

ASJC Scopus subject areas

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