Tumor necrosis factor receptor p55 and p75 deficiency protects mice from developing experimental autoimmune myasthenia gravis

Elzbieta Goluszko; Caishu Deng; Mathilde A. Poussin; Premkumar Christadoss

doi:10.1016/S0165-5728(01)00474-X

Tumor necrosis factor receptor p55 and p75 deficiency protects mice from developing experimental autoimmune myasthenia gravis

Elzbieta Goluszko
, Caishu Deng
, Mathilde A. Poussin
, Premkumar Christadoss

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

34 Scopus citations

Abstract

The precise pathogenic role of proinflammatory cytokines belonging to the tumor necrosis factor (TNF) family has not been investigated yet in antibody-mediated myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG). In this study we report that TNF receptor p55^-/- p75^-/- mice were resistant to the development of clinical EAMG induced by acetylcholine receptor (AChR) immunizations. The resistance was associated with reduced serum levels of IgG, IgG₁, IgG_2a, and IgG_2b anti-AChR antibody isotypes. However, IgM anti-AChR antibodies were not reduced, suggesting defective anti-AChR IgG class switching in TNF receptor p55^-/- p75^-/- mice. We thus demonstrate the genetic evidence for the role of TNF receptor p55 and p75 in EAMG pathogenesis, and their requirement for the generation of anti-AChR IgG antibodies.

Original language	English (US)
Pages (from-to)	85-93
Number of pages	9
Journal	Journal of Neuroimmunology
Volume	122
Issue number	1-2
DOIs	https://doi.org/10.1016/S0165-5728(01)00474-X
State	Published - 2002
Externally published	Yes

Keywords

Autoimmunity
Lymphotoxin-α
Myasthenia gravis
TNF receptors
TNF-α

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

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10.1016/S0165-5728(01)00474-X

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title = "Tumor necrosis factor receptor p55 and p75 deficiency protects mice from developing experimental autoimmune myasthenia gravis",

abstract = "The precise pathogenic role of proinflammatory cytokines belonging to the tumor necrosis factor (TNF) family has not been investigated yet in antibody-mediated myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG). In this study we report that TNF receptor p55-/- p75-/- mice were resistant to the development of clinical EAMG induced by acetylcholine receptor (AChR) immunizations. The resistance was associated with reduced serum levels of IgG, IgG1, IgG2a, and IgG2b anti-AChR antibody isotypes. However, IgM anti-AChR antibodies were not reduced, suggesting defective anti-AChR IgG class switching in TNF receptor p55-/- p75-/- mice. We thus demonstrate the genetic evidence for the role of TNF receptor p55 and p75 in EAMG pathogenesis, and their requirement for the generation of anti-AChR IgG antibodies.",

keywords = "Autoimmunity, Lymphotoxin-α, Myasthenia gravis, TNF receptors, TNF-α",

author = "Elzbieta Goluszko and Caishu Deng and Poussin, \{Mathilde A.\} and Premkumar Christadoss",

note = "Funding Information: We thank Immunex, Seattle, WA, for providing us TNFR p55 −/− p75 −/− mice, and Mardelle Susman for editing the manuscript. This study was supported by Muscular Dystrophy Association and Association Francaise Contre les Myopathies. M. Poussin has a consecutive postdoctoral fellowship from the Association Francaise Contre les Myopathies, MG Foundation of America, and James W. McLaughlin Foundation. C. Deng was a James W. McLaughlin Foundation Postdoctoral Fellow.",

year = "2002",

doi = "10.1016/S0165-5728(01)00474-X",

language = "English (US)",

volume = "122",

pages = "85--93",

journal = "Journal of Neuroimmunology",

issn = "0165-5728",

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AU - Goluszko, Elzbieta

AU - Deng, Caishu

AU - Poussin, Mathilde A.

AU - Christadoss, Premkumar

N1 - Funding Information: We thank Immunex, Seattle, WA, for providing us TNFR p55 −/− p75 −/− mice, and Mardelle Susman for editing the manuscript. This study was supported by Muscular Dystrophy Association and Association Francaise Contre les Myopathies. M. Poussin has a consecutive postdoctoral fellowship from the Association Francaise Contre les Myopathies, MG Foundation of America, and James W. McLaughlin Foundation. C. Deng was a James W. McLaughlin Foundation Postdoctoral Fellow.

PY - 2002

Y1 - 2002

N2 - The precise pathogenic role of proinflammatory cytokines belonging to the tumor necrosis factor (TNF) family has not been investigated yet in antibody-mediated myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG). In this study we report that TNF receptor p55-/- p75-/- mice were resistant to the development of clinical EAMG induced by acetylcholine receptor (AChR) immunizations. The resistance was associated with reduced serum levels of IgG, IgG1, IgG2a, and IgG2b anti-AChR antibody isotypes. However, IgM anti-AChR antibodies were not reduced, suggesting defective anti-AChR IgG class switching in TNF receptor p55-/- p75-/- mice. We thus demonstrate the genetic evidence for the role of TNF receptor p55 and p75 in EAMG pathogenesis, and their requirement for the generation of anti-AChR IgG antibodies.

AB - The precise pathogenic role of proinflammatory cytokines belonging to the tumor necrosis factor (TNF) family has not been investigated yet in antibody-mediated myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG). In this study we report that TNF receptor p55-/- p75-/- mice were resistant to the development of clinical EAMG induced by acetylcholine receptor (AChR) immunizations. The resistance was associated with reduced serum levels of IgG, IgG1, IgG2a, and IgG2b anti-AChR antibody isotypes. However, IgM anti-AChR antibodies were not reduced, suggesting defective anti-AChR IgG class switching in TNF receptor p55-/- p75-/- mice. We thus demonstrate the genetic evidence for the role of TNF receptor p55 and p75 in EAMG pathogenesis, and their requirement for the generation of anti-AChR IgG antibodies.

KW - Autoimmunity

KW - Lymphotoxin-α

KW - Myasthenia gravis

KW - TNF receptors

KW - TNF-α

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Tumor necrosis factor receptor p55 and p75 deficiency protects mice from developing experimental autoimmune myasthenia gravis

Abstract

Keywords

ASJC Scopus subject areas

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