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 journalArticle

34 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)85-93
Number of pages9
JournalJournal of Neuroimmunology
Volume122
Issue number1-2
DOIs
StatePublished - 2002

Fingerprint

Autoimmune Experimental Myasthenia Gravis
Tumor Necrosis Factor Receptors
Cholinergic Receptors
Immunoglobulin G
Antibodies
Immunoglobulin Class Switching
Immunization
Tumor Necrosis Factor-alpha
Cytokines
Serum

Keywords

  • Autoimmunity
  • Lymphotoxin-α
  • Myasthenia gravis
  • TNF receptors
  • TNF-α

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

Cite this

Tumor necrosis factor receptor p55 and p75 deficiency protects mice from developing experimental autoimmune myasthenia gravis. / Goluszko, Elzbieta; Deng, Caishu; Poussin, Mathilde A.; Christadoss, Premkumar.

In: Journal of Neuroimmunology, Vol. 122, No. 1-2, 2002, p. 85-93.

Research output: Contribution to journalArticle

Goluszko, Elzbieta ; Deng, Caishu ; Poussin, Mathilde A. ; Christadoss, Premkumar. / Tumor necrosis factor receptor p55 and p75 deficiency protects mice from developing experimental autoimmune myasthenia gravis. In: Journal of Neuroimmunology. 2002 ; Vol. 122, No. 1-2. pp. 85-93.
@article{1c69c2256ee1478c8cd3c036021d0d94,
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",
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",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - Tumor necrosis factor receptor p55 and p75 deficiency protects mice from developing experimental autoimmune myasthenia gravis

AU - Goluszko, Elzbieta

AU - Deng, Caishu

AU - Poussin, Mathilde A.

AU - Christadoss, Premkumar

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

UR - http://www.scopus.com/inward/record.url?scp=0036147552&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036147552&partnerID=8YFLogxK

U2 - 10.1016/S0165-5728(01)00474-X

DO - 10.1016/S0165-5728(01)00474-X

M3 - Article

C2 - 11777546

AN - SCOPUS:0036147552

VL - 122

SP - 85

EP - 93

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

SN - 0165-5728

IS - 1-2

ER -