Antibody-mediated remyelination operates through mechanism independent of immunomodulation

Bogoljub Ciric; Virginia Van Keulen; Mateo Paz Soldan; Moses Rodriguez; Larry R. Pease

doi:10.1016/j.jneuroim.2003.11.002

Antibody-mediated remyelination operates through mechanism independent of immunomodulation

Bogoljub Ciric, Virginia Van Keulen, Mateo Paz Soldan, Moses Rodriguez, Larry R. Pease

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

32 Scopus citations

Abstract

A set of antibodies capable of binding glial cells promotes remyelination in models of multiple sclerosis (MS). Within this set, the mouse antibody, SCH94.03, was immunomodulatory implying that immune system mobilization might be integral to remyelination. We evaluated whether the human remyelination-promoting antibody rHIgM22 influences acquired immunity. The antibody did not bind to immune cells, or influence humoral immune responses, antigen presentation, T cell proliferation or cytokine production. Treatment with rHIgM22 had no effect on demyelination or virus infection in two disease models. These results demonstrate that the remyelination-promoting activity of antibody rHIgM22 is not dependent on immunomodulation.

Original language	English (US)
Pages (from-to)	153-161
Number of pages	9
Journal	Journal of neuroimmunology
Volume	146
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2003.11.002
State	Published - Jan 2004

Keywords

EAE
IgM
Immunomodulation
Multiple sclerosis
Remyelination

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

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10.1016/j.jneuroim.2003.11.002

Cite this

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title = "Antibody-mediated remyelination operates through mechanism independent of immunomodulation",

abstract = "A set of antibodies capable of binding glial cells promotes remyelination in models of multiple sclerosis (MS). Within this set, the mouse antibody, SCH94.03, was immunomodulatory implying that immune system mobilization might be integral to remyelination. We evaluated whether the human remyelination-promoting antibody rHIgM22 influences acquired immunity. The antibody did not bind to immune cells, or influence humoral immune responses, antigen presentation, T cell proliferation or cytokine production. Treatment with rHIgM22 had no effect on demyelination or virus infection in two disease models. These results demonstrate that the remyelination-promoting activity of antibody rHIgM22 is not dependent on immunomodulation.",

keywords = "EAE, IgM, Immunomodulation, Multiple sclerosis, Remyelination",

author = "Bogoljub Ciric and {Van Keulen}, Virginia and {Paz Soldan}, Mateo and Moses Rodriguez and Pease, {Larry R.}",

note = "Funding Information: We thank Mr. and Mrs. E. Applebaum for their generous support. This work was supported by NIH grant RO1-NS24180 and Acorda Therapeutics.",

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AU - Ciric, Bogoljub

AU - Van Keulen, Virginia

AU - Paz Soldan, Mateo

AU - Rodriguez, Moses

AU - Pease, Larry R.

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AB - A set of antibodies capable of binding glial cells promotes remyelination in models of multiple sclerosis (MS). Within this set, the mouse antibody, SCH94.03, was immunomodulatory implying that immune system mobilization might be integral to remyelination. We evaluated whether the human remyelination-promoting antibody rHIgM22 influences acquired immunity. The antibody did not bind to immune cells, or influence humoral immune responses, antigen presentation, T cell proliferation or cytokine production. Treatment with rHIgM22 had no effect on demyelination or virus infection in two disease models. These results demonstrate that the remyelination-promoting activity of antibody rHIgM22 is not dependent on immunomodulation.

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KW - Immunomodulation

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KW - Remyelination

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Antibody-mediated remyelination operates through mechanism independent of immunomodulation

Abstract

Keywords

ASJC Scopus subject areas

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