Suppression of experimental autoimmune myasthenia gravis in IL-10 gene-disrupted mice is associated with reduced B cells and serum cytotoxicity on mouse cell line expressing AChR

Mathilde A. Poussin, Elzbieta Goluszko, Thomas K. Hughes, Sacha I. Duchicella, Premkumar Christadoss

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

To analyze the role of interleukin-10 (IL-10) in experimental autoimmune myasthenia gravis (EAMG) pathogenesis, we induced clinical EAMG in C57BL/6 and IL-10 gene-knockout (KO) mice. IL-10 KO mice had a lower incidence and severity of EAMG, with less muscle acetylcholine receptor (AChR) loss. AChR-immunized IL-10 KO mice showed a significantly higher AChR-specific proliferative response, altered cytokine response, lower number of class II-positive cells and B-cells, but a greater CD5+CD19+ population than C57BL/6 mice. The lower clinical incidence in IL-10 KO could be explained not by a reduction of the quantity, but by a possible difference in the pathogenicity of anti-AChR antibodies. Copyright (C) 2000.

Original languageEnglish (US)
Pages (from-to)152-160
Number of pages9
JournalJournal of Neuroimmunology
Volume111
Issue number1-2
DOIs
StatePublished - Nov 1 2000

Fingerprint

Autoimmune Experimental Myasthenia Gravis
Cholinergic Receptors
Interleukin-10
B-Lymphocytes
Cell Line
Knockout Mice
Serum
Genes
Gene Knockout Techniques
Incidence
Inbred C57BL Mouse
Virulence
Cytokines
Muscles
Antibodies
Population

Keywords

  • Autoimmunity
  • IL-10
  • IL-10 gene knockout
  • Immunomodulation
  • Myasthenia gravis

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

Cite this

Suppression of experimental autoimmune myasthenia gravis in IL-10 gene-disrupted mice is associated with reduced B cells and serum cytotoxicity on mouse cell line expressing AChR. / Poussin, Mathilde A.; Goluszko, Elzbieta; Hughes, Thomas K.; Duchicella, Sacha I.; Christadoss, Premkumar.

In: Journal of Neuroimmunology, Vol. 111, No. 1-2, 01.11.2000, p. 152-160.

Research output: Contribution to journalArticle

Poussin, Mathilde A. ; Goluszko, Elzbieta ; Hughes, Thomas K. ; Duchicella, Sacha I. ; Christadoss, Premkumar. / Suppression of experimental autoimmune myasthenia gravis in IL-10 gene-disrupted mice is associated with reduced B cells and serum cytotoxicity on mouse cell line expressing AChR. In: Journal of Neuroimmunology. 2000 ; Vol. 111, No. 1-2. pp. 152-160.
@article{18f32c6ab6aa4439bbe270fef2a29a08,
title = "Suppression of experimental autoimmune myasthenia gravis in IL-10 gene-disrupted mice is associated with reduced B cells and serum cytotoxicity on mouse cell line expressing AChR",
abstract = "To analyze the role of interleukin-10 (IL-10) in experimental autoimmune myasthenia gravis (EAMG) pathogenesis, we induced clinical EAMG in C57BL/6 and IL-10 gene-knockout (KO) mice. IL-10 KO mice had a lower incidence and severity of EAMG, with less muscle acetylcholine receptor (AChR) loss. AChR-immunized IL-10 KO mice showed a significantly higher AChR-specific proliferative response, altered cytokine response, lower number of class II-positive cells and B-cells, but a greater CD5+CD19+ population than C57BL/6 mice. The lower clinical incidence in IL-10 KO could be explained not by a reduction of the quantity, but by a possible difference in the pathogenicity of anti-AChR antibodies. Copyright (C) 2000.",
keywords = "Autoimmunity, IL-10, IL-10 gene knockout, Immunomodulation, Myasthenia gravis",
author = "Poussin, {Mathilde A.} and Elzbieta Goluszko and Hughes, {Thomas K.} and Duchicella, {Sacha I.} and Premkumar Christadoss",
year = "2000",
month = "11",
day = "1",
doi = "10.1016/S0165-5728(00)00385-4",
language = "English (US)",
volume = "111",
pages = "152--160",
journal = "Journal of Neuroimmunology",
issn = "0165-5728",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - Suppression of experimental autoimmune myasthenia gravis in IL-10 gene-disrupted mice is associated with reduced B cells and serum cytotoxicity on mouse cell line expressing AChR

AU - Poussin, Mathilde A.

AU - Goluszko, Elzbieta

AU - Hughes, Thomas K.

AU - Duchicella, Sacha I.

AU - Christadoss, Premkumar

PY - 2000/11/1

Y1 - 2000/11/1

N2 - To analyze the role of interleukin-10 (IL-10) in experimental autoimmune myasthenia gravis (EAMG) pathogenesis, we induced clinical EAMG in C57BL/6 and IL-10 gene-knockout (KO) mice. IL-10 KO mice had a lower incidence and severity of EAMG, with less muscle acetylcholine receptor (AChR) loss. AChR-immunized IL-10 KO mice showed a significantly higher AChR-specific proliferative response, altered cytokine response, lower number of class II-positive cells and B-cells, but a greater CD5+CD19+ population than C57BL/6 mice. The lower clinical incidence in IL-10 KO could be explained not by a reduction of the quantity, but by a possible difference in the pathogenicity of anti-AChR antibodies. Copyright (C) 2000.

AB - To analyze the role of interleukin-10 (IL-10) in experimental autoimmune myasthenia gravis (EAMG) pathogenesis, we induced clinical EAMG in C57BL/6 and IL-10 gene-knockout (KO) mice. IL-10 KO mice had a lower incidence and severity of EAMG, with less muscle acetylcholine receptor (AChR) loss. AChR-immunized IL-10 KO mice showed a significantly higher AChR-specific proliferative response, altered cytokine response, lower number of class II-positive cells and B-cells, but a greater CD5+CD19+ population than C57BL/6 mice. The lower clinical incidence in IL-10 KO could be explained not by a reduction of the quantity, but by a possible difference in the pathogenicity of anti-AChR antibodies. Copyright (C) 2000.

KW - Autoimmunity

KW - IL-10

KW - IL-10 gene knockout

KW - Immunomodulation

KW - Myasthenia gravis

UR - http://www.scopus.com/inward/record.url?scp=0034333062&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034333062&partnerID=8YFLogxK

U2 - 10.1016/S0165-5728(00)00385-4

DO - 10.1016/S0165-5728(00)00385-4

M3 - Article

C2 - 11063833

AN - SCOPUS:0034333062

VL - 111

SP - 152

EP - 160

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

SN - 0165-5728

IS - 1-2

ER -