Acetylcholine receptor-reactive antibody induces nitric oxide production by a rat skeletal muscle cell line: Influence of cytokine environment

Yvonne R. Garcia; Jennifer J. May; Alicia M. Green; Keith A. Krolick

doi:10.1016/S0165-5728(01)00414-3

Acetylcholine receptor-reactive antibody induces nitric oxide production by a rat skeletal muscle cell line: Influence of cytokine environment

Yvonne R. Garcia, Jennifer J. May, Alicia M. Green, Keith A. Krolick

Microbiology, Immunology & Molecular Genetics

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

10 Scopus citations

Abstract

The monoclonal Lewis rat skeletal muscle cell line, LE1, responded to the acetylcholine receptor (AChR)-reactive antibody mAb35 by up-regulating levels of mRNA for inducible nitric oxide synthase (iNOS/NOS-II), followed by levels of NO. Interferon-gamma (IFN-γ) and interleukin-1 (IL-1) were also each capable of inducing iNOS message, and synergistically with mAb35. Finally, myocyte-derived NO was implicated as a possible source of immunomodulation in experimental autoimmune myasthenia gravis (EAMG), as shown by the ability of the culture fluids from IFN-γ-activated LE1 cells to inhibit the proliferation of AChR-reactive T cells.

Original language	English (US)
Pages (from-to)	103-111
Number of pages	9
Journal	Journal of Neuroimmunology
Volume	120
Issue number	1-2
DOIs	https://doi.org/10.1016/S0165-5728(01)00414-3
State	Published - 2001

Keywords

Autoimmune disease
Experimental autoimmune myasthenia gravis
Inflammatory cytokines
Nitric oxide synthase

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

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@article{321cfc1f8a954dd4b97542a9f9032346,

title = "Acetylcholine receptor-reactive antibody induces nitric oxide production by a rat skeletal muscle cell line: Influence of cytokine environment",

abstract = "The monoclonal Lewis rat skeletal muscle cell line, LE1, responded to the acetylcholine receptor (AChR)-reactive antibody mAb35 by up-regulating levels of mRNA for inducible nitric oxide synthase (iNOS/NOS-II), followed by levels of NO. Interferon-gamma (IFN-γ) and interleukin-1 (IL-1) were also each capable of inducing iNOS message, and synergistically with mAb35. Finally, myocyte-derived NO was implicated as a possible source of immunomodulation in experimental autoimmune myasthenia gravis (EAMG), as shown by the ability of the culture fluids from IFN-γ-activated LE1 cells to inhibit the proliferation of AChR-reactive T cells.",

keywords = "Autoimmune disease, Experimental autoimmune myasthenia gravis, Inflammatory cytokines, Nitric oxide synthase",

author = "Garcia, {Yvonne R.} and May, {Jennifer J.} and Green, {Alicia M.} and Krolick, {Keith A.}",

note = "Funding Information: This research was supported by a grant from the National Institutes of Health (R01 NS/AI 36313, NS38904 and NS42116). We express our thanks to Irma Gonzales for her technical support, and to Dr. Y. Mulhern for many helpful discussions.",

year = "2001",

doi = "10.1016/S0165-5728(01)00414-3",

language = "English (US)",

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T2 - Influence of cytokine environment

AU - Garcia, Yvonne R.

AU - May, Jennifer J.

AU - Green, Alicia M.

AU - Krolick, Keith A.

N1 - Funding Information: This research was supported by a grant from the National Institutes of Health (R01 NS/AI 36313, NS38904 and NS42116). We express our thanks to Irma Gonzales for her technical support, and to Dr. Y. Mulhern for many helpful discussions.

PY - 2001

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N2 - The monoclonal Lewis rat skeletal muscle cell line, LE1, responded to the acetylcholine receptor (AChR)-reactive antibody mAb35 by up-regulating levels of mRNA for inducible nitric oxide synthase (iNOS/NOS-II), followed by levels of NO. Interferon-gamma (IFN-γ) and interleukin-1 (IL-1) were also each capable of inducing iNOS message, and synergistically with mAb35. Finally, myocyte-derived NO was implicated as a possible source of immunomodulation in experimental autoimmune myasthenia gravis (EAMG), as shown by the ability of the culture fluids from IFN-γ-activated LE1 cells to inhibit the proliferation of AChR-reactive T cells.

AB - The monoclonal Lewis rat skeletal muscle cell line, LE1, responded to the acetylcholine receptor (AChR)-reactive antibody mAb35 by up-regulating levels of mRNA for inducible nitric oxide synthase (iNOS/NOS-II), followed by levels of NO. Interferon-gamma (IFN-γ) and interleukin-1 (IL-1) were also each capable of inducing iNOS message, and synergistically with mAb35. Finally, myocyte-derived NO was implicated as a possible source of immunomodulation in experimental autoimmune myasthenia gravis (EAMG), as shown by the ability of the culture fluids from IFN-γ-activated LE1 cells to inhibit the proliferation of AChR-reactive T cells.

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