Interferon-beta-1a treatment increases CD56bright natural killer cells and CD4+CD25+ Foxp3 expression in subjects with multiple sclerosis

Arthur A. Vandenbark; Jianya Huan; Marisa Agotsch; Dorian La Tocha; Susan Goelz; Halina Offner; Stefan Lanker; Dennis Bourdette

doi:10.1016/j.jneuroim.2009.08.007

Interferon-beta-1a treatment increases CD56^bright natural killer cells and CD4+CD25+ Foxp3 expression in subjects with multiple sclerosis

Arthur A. Vandenbark, Jianya Huan, Marisa Agotsch, Dorian La Tocha, Susan Goelz, Halina Offner, Stefan Lanker, Dennis Bourdette

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

87 Scopus citations

Abstract

Disease modifying effects of interferon (IFN)-β therapy in patients with multiple sclerosis (MS) may be mediated in part through enhanced immunoregulation by the CD56^bright subpopulation of natural killer (NK) cells and by Foxp3+ (not italicized) CD4+CD25+ regulatory T cells (Treg). We found that IFN-β-1a(IM) treatment of relapsing-remitting (RR)MS subjects over 12 months significantly increased both percentage of CD56^bright NK cells and Foxp3 mRNA expression compared to baseline values, untreated RRMS subjects and healthy controls (HC). This striking enhancement of two prominent immunoregulatory pathways lends support to the idea that beneficial effects of IFN-β-1a in MS include control of pernicious autoimmunity.

Original language	English (US)
Pages (from-to)	125-128
Number of pages	4
Journal	Journal of Neuroimmunology
Volume	215
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2009.08.007
State	Published - Oct 30 2009

Keywords

CD56 NK cells
Foxp3 expression
IFN-β-1a
Multiple sclerosis

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

Access to Document

10.1016/j.jneuroim.2009.08.007

Cite this

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title = "Interferon-beta-1a treatment increases CD56bright natural killer cells and CD4+CD25+ Foxp3 expression in subjects with multiple sclerosis",

abstract = "Disease modifying effects of interferon (IFN)-β therapy in patients with multiple sclerosis (MS) may be mediated in part through enhanced immunoregulation by the CD56bright subpopulation of natural killer (NK) cells and by Foxp3+ (not italicized) CD4+CD25+ regulatory T cells (Treg). We found that IFN-β-1a(IM) treatment of relapsing-remitting (RR)MS subjects over 12 months significantly increased both percentage of CD56bright NK cells and Foxp3 mRNA expression compared to baseline values, untreated RRMS subjects and healthy controls (HC). This striking enhancement of two prominent immunoregulatory pathways lends support to the idea that beneficial effects of IFN-β-1a in MS include control of pernicious autoimmunity.",

keywords = "CD56 NK cells, Foxp3 expression, IFN-β-1a, Multiple sclerosis",

author = "Vandenbark, {Arthur A.} and Jianya Huan and Marisa Agotsch and {La Tocha}, Dorian and Susan Goelz and Halina Offner and Stefan Lanker and Dennis Bourdette",

note = "Funding Information: This study was supported by Biogen-Idec , The Nancy Davis MS Center Without Walls and the Department of Veterans Affairs Department of Biomedical Research . The authors wish to thank Stacie Moultrie (clinical coordinator at the MS Center of Oregon), and Ms. Eva Niehaus for assistance in preparing the manuscript.",

year = "2009",

month = oct,

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doi = "10.1016/j.jneuroim.2009.08.007",

language = "English (US)",

volume = "215",

pages = "125--128",

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T1 - Interferon-beta-1a treatment increases CD56bright natural killer cells and CD4+CD25+ Foxp3 expression in subjects with multiple sclerosis

AU - Vandenbark, Arthur A.

AU - Huan, Jianya

AU - Agotsch, Marisa

AU - La Tocha, Dorian

AU - Goelz, Susan

AU - Offner, Halina

AU - Lanker, Stefan

AU - Bourdette, Dennis

N1 - Funding Information: This study was supported by Biogen-Idec , The Nancy Davis MS Center Without Walls and the Department of Veterans Affairs Department of Biomedical Research . The authors wish to thank Stacie Moultrie (clinical coordinator at the MS Center of Oregon), and Ms. Eva Niehaus for assistance in preparing the manuscript.

PY - 2009/10/30

Y1 - 2009/10/30

N2 - Disease modifying effects of interferon (IFN)-β therapy in patients with multiple sclerosis (MS) may be mediated in part through enhanced immunoregulation by the CD56bright subpopulation of natural killer (NK) cells and by Foxp3+ (not italicized) CD4+CD25+ regulatory T cells (Treg). We found that IFN-β-1a(IM) treatment of relapsing-remitting (RR)MS subjects over 12 months significantly increased both percentage of CD56bright NK cells and Foxp3 mRNA expression compared to baseline values, untreated RRMS subjects and healthy controls (HC). This striking enhancement of two prominent immunoregulatory pathways lends support to the idea that beneficial effects of IFN-β-1a in MS include control of pernicious autoimmunity.

AB - Disease modifying effects of interferon (IFN)-β therapy in patients with multiple sclerosis (MS) may be mediated in part through enhanced immunoregulation by the CD56bright subpopulation of natural killer (NK) cells and by Foxp3+ (not italicized) CD4+CD25+ regulatory T cells (Treg). We found that IFN-β-1a(IM) treatment of relapsing-remitting (RR)MS subjects over 12 months significantly increased both percentage of CD56bright NK cells and Foxp3 mRNA expression compared to baseline values, untreated RRMS subjects and healthy controls (HC). This striking enhancement of two prominent immunoregulatory pathways lends support to the idea that beneficial effects of IFN-β-1a in MS include control of pernicious autoimmunity.

KW - CD56 NK cells

KW - Foxp3 expression

KW - IFN-β-1a

KW - Multiple sclerosis

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