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

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 - Nov 10 2001

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Keywords

Autoimmune disease
Experimental autoimmune myasthenia gravis
Inflammatory cytokines
Nitric oxide synthase

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

Cite this

Garcia, Y. R., May, J. J., Green, A. M., & Krolick, K. A. (2001). Acetylcholine receptor-reactive antibody induces nitric oxide production by a rat skeletal muscle cell line: Influence of cytokine environment. Journal of Neuroimmunology, 120(1-2), 103-111. https://doi.org/10.1016/S0165-5728(01)00414-3

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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.",

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10.1016/S0165-5728(01)00414-3