Glatiramer Acetate Biases Dendritic Cells Towards an Anti-Inflammatory Phenotype by Modulating OPN, IL-17, and RORγt Responses and by Increasing IL-10 Production in Experimental Allergic Encephalomyelitis

Sakhina Begum-Haque; Marc Christy; Yan Wang; Eli Kasper; Javier Ochoa-Reparaz; Jacqueline Y. Smith; Azizul Haque; Lloyd H. Kasper

doi:10.1016/j.jneuroim.2012.10.003

Glatiramer Acetate Biases Dendritic Cells Towards an Anti-Inflammatory Phenotype by Modulating OPN, IL-17, and RORγt Responses and by Increasing IL-10 Production in Experimental Allergic Encephalomyelitis

Sakhina Begum-Haque, Marc Christy, Yan Wang, Eli Kasper, Javier Ochoa-Reparaz, Jacqueline Y. Smith, Azizul Haque, Lloyd H. Kasper

Geisel Medical School at Dartmouth

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

18 Scopus citations

Abstract

Paralleling our previous mechanistic studies of glatiramer acetate (GA; Copaxone) activity, we show that GA curbs the expression of Toll-like receptor (TLR) 9 and the universal adapter protein Myd88 in mice with EAE, the animal model for multiple sclerosis. Concurrent with enhanced dendritic cell (DC) production of IL-10, GA interferes with OPN, IL-17, and ROR gamma expression in DCs of mice with EAE, and suppresses brain expression of the EAE-induced chemokines, MIP1α and β, IP-10 and RANTES. Thus GA not only biases dendritic cells towards an anti-inflammatory phenotype, but also suppresses the expression of factors that affect the blood–brain barrier penetration during neuroinflammation.

Original language	American English
Pages (from-to)	117-24
Number of pages	8
Journal	Journal of Neuroimmunology
Volume	254
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2012.10.003
State	Published - 15 Jan 2013
Externally published	Yes

Keywords

EAE
GA
IL-10
chemokines
dendritic cells
osteopontin

EGS Disciplines

Biology

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Begum-Haque, S., Christy, M., Wang, Y., Kasper, E., Ochoa-Reparaz, J., Smith, J. Y., Haque, A., & Kasper, L. H. (2013). Glatiramer Acetate Biases Dendritic Cells Towards an Anti-Inflammatory Phenotype by Modulating OPN, IL-17, and RORγt Responses and by Increasing IL-10 Production in Experimental Allergic Encephalomyelitis. Journal of Neuroimmunology, 254(1-2), 117-24. https://doi.org/10.1016/j.jneuroim.2012.10.003

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title = "Glatiramer Acetate Biases Dendritic Cells Towards an Anti-Inflammatory Phenotype by Modulating OPN, IL-17, and RORγt Responses and by Increasing IL-10 Production in Experimental Allergic Encephalomyelitis",

abstract = " Paralleling our previous mechanistic studies of glatiramer acetate (GA; Copaxone) activity, we show that GA curbs the expression of Toll-like receptor (TLR) 9 and the universal adapter protein Myd88 in mice with EAE, the animal model for multiple sclerosis. Concurrent with enhanced dendritic cell (DC) production of IL-10, GA interferes with OPN, IL-17, and ROR gamma expression in DCs of mice with EAE, and suppresses brain expression of the EAE-induced chemokines, MIP1α and β, IP-10 and RANTES. Thus GA not only biases dendritic cells towards an anti-inflammatory phenotype, but also suppresses the expression of factors that affect the blood–brain barrier penetration during neuroinflammation. ",

keywords = "EAE, GA, IL-10, chemokines, dendritic cells, osteopontin",

author = "Sakhina Begum-Haque and Marc Christy and Yan Wang and Eli Kasper and Javier Ochoa-Reparaz and Smith, {Jacqueline Y.} and Azizul Haque and Kasper, {Lloyd H.}",

year = "2013",

month = jan,

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doi = "10.1016/j.jneuroim.2012.10.003",

language = "American English",

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Begum-Haque, S, Christy, M, Wang, Y, Kasper, E, Ochoa-Reparaz, J, Smith, JY, Haque, A & Kasper, LH 2013, 'Glatiramer Acetate Biases Dendritic Cells Towards an Anti-Inflammatory Phenotype by Modulating OPN, IL-17, and RORγt Responses and by Increasing IL-10 Production in Experimental Allergic Encephalomyelitis', Journal of Neuroimmunology, vol. 254, no. 1-2, pp. 117-24. https://doi.org/10.1016/j.jneuroim.2012.10.003

Glatiramer Acetate Biases Dendritic Cells Towards an Anti-Inflammatory Phenotype by Modulating OPN, IL-17, and RORγt Responses and by Increasing IL-10 Production in Experimental Allergic Encephalomyelitis. / Begum-Haque, Sakhina; Christy, Marc; Wang, Yan et al.
In: Journal of Neuroimmunology, Vol. 254, No. 1-2, 15.01.2013, p. 117-24.

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

TY - JOUR

T1 - Glatiramer Acetate Biases Dendritic Cells Towards an Anti-Inflammatory Phenotype by Modulating OPN, IL-17, and RORγt Responses and by Increasing IL-10 Production in Experimental Allergic Encephalomyelitis

AU - Begum-Haque, Sakhina

AU - Christy, Marc

AU - Wang, Yan

AU - Kasper, Eli

AU - Ochoa-Reparaz, Javier

AU - Smith, Jacqueline Y.

AU - Haque, Azizul

AU - Kasper, Lloyd H.

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N2 - Paralleling our previous mechanistic studies of glatiramer acetate (GA; Copaxone) activity, we show that GA curbs the expression of Toll-like receptor (TLR) 9 and the universal adapter protein Myd88 in mice with EAE, the animal model for multiple sclerosis. Concurrent with enhanced dendritic cell (DC) production of IL-10, GA interferes with OPN, IL-17, and ROR gamma expression in DCs of mice with EAE, and suppresses brain expression of the EAE-induced chemokines, MIP1α and β, IP-10 and RANTES. Thus GA not only biases dendritic cells towards an anti-inflammatory phenotype, but also suppresses the expression of factors that affect the blood–brain barrier penetration during neuroinflammation.

AB - Paralleling our previous mechanistic studies of glatiramer acetate (GA; Copaxone) activity, we show that GA curbs the expression of Toll-like receptor (TLR) 9 and the universal adapter protein Myd88 in mice with EAE, the animal model for multiple sclerosis. Concurrent with enhanced dendritic cell (DC) production of IL-10, GA interferes with OPN, IL-17, and ROR gamma expression in DCs of mice with EAE, and suppresses brain expression of the EAE-induced chemokines, MIP1α and β, IP-10 and RANTES. Thus GA not only biases dendritic cells towards an anti-inflammatory phenotype, but also suppresses the expression of factors that affect the blood–brain barrier penetration during neuroinflammation.

KW - EAE

KW - GA

KW - IL-10

KW - chemokines

KW - dendritic cells

KW - osteopontin

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DO - 10.1016/j.jneuroim.2012.10.003

M3 - Article

C2 - 23141166

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JO - Journal of Neuroimmunology

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ER -

Begum-Haque S, Christy M, Wang Y, Kasper E, Ochoa-Reparaz J, Smith JY et al. Glatiramer Acetate Biases Dendritic Cells Towards an Anti-Inflammatory Phenotype by Modulating OPN, IL-17, and RORγt Responses and by Increasing IL-10 Production in Experimental Allergic Encephalomyelitis. Journal of Neuroimmunology. 2013 Jan 15;254(1-2):117-24. doi: 10.1016/j.jneuroim.2012.10.003